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THE  NATURAL  HISTORY 
OF  DISEASE 


Oxford  University  Press,  Amen  House,  London  E.O.  4 

GLASGOW  SIW  TOSK  TORONTO  JCELBOCESE  WSLUS0TO5 
BOMBAY  CALCUTTA  MADRAS  CAPE  TOWS 

Geoffrey  Cumberlege,  Publisher  to  the  University 


OXFORD  MEDICAL  PUBLICATIONS 


THE 

NATURAL  HISTORY 
OF  DISEASE 


BY 

JOHN  A.  RYLE 


Proftnor  of  Social  Medicine  in  the  U nicer!  Uy 
of  Oxford 

Conrulling  Phyrteian  la  Gvy'e  II capital,  London, 
and  the  BaicUffe  Infirmary,  Oxford 
Formerly  Bigiui  Preftuor  of  Phytic  in  the 
Unintreity  of  Cambridge 


SECOND  EDITION 


GEOFFREY  CUMBERLEGE 
OXFORD  UNIVERSITY  PRESS 

LONDON  NEW  YORK  TORONTO 


*In  writing,  therefore,  a history  of  diseases,  every  philo- 
sophical hypothesis  which  Jiath  prepossessed  the  writer 
in  its  favour,  ought  to  be  totally  Laid  aside,  and  then  the 
manifest  and  natural  phenomena  of  diseases,  however 
minute,  must  be  noted  with  the  utmost  accuracy,  imitat- 
ing in  this  the  great  exactness  of  painters,  who  in  their 
pictures  copy  the  smallest  spots  or  moles  in  the  originals ; 
for  it  is  difficult  to  give  a detail  of  the  numerous  errors 
that  spring  from  hypothesis. . . 

THOMAS  SYDENHAM 

(From  The  Works  of  Thomas  Sydenham,  3/.D.) 


* Symptoms  are  universally  available;  they  are  the  voice 
of  nature;  signs,  by  which  I mean  more  artificial  and 
refined  methods  of  scrutiny — the  stethoscope,  the  micro- 
scope, &e. — are  not  always  within  the  power  of  every 
man,  and  with  alt  their  help,  arc  additions, 
not  substitutes.’ 

JOHN  DROWN 

(From  the  Introduction  to  Horae  Subsecioae) 

‘Every  pain  has  its  distinct  and  pregnant  signification, 
if  we  will  but  carefully  search  for  it.’ 

JOHN  mrroN 

( Lectures  on  'Rest  and  Pain') 


Second  .Edition  1018 
Second  Impression  1019 

wn-rni  ts  GREAT  BRITAIN  AT  THE  UNTTZRSU*  PRESS,  OXFORD 
BT  rw  mr.rs  BiTET,  PRINTER  TO  THE  rs-TVERSrrr 


TO 

A.F.  H. 

IN  FRIENDSHIP  AND 
GRATITUDE 
FOR  MUCH 
INSPIRATION 


PREFACE  TO  THE  SECOND  EDITION 

A little  over  a decade  has  passed  since  this  book  was  pub- 
lished. It  has,  I gather,  had  quite  a number  of  friends. 
Although  the  original  issue  was  by  then  exhausted,  the 
publication  of  a second  impression  during  the  war  was 
rendered  impossible  by  reason  of  the  paper  shortage.  The 
publishers  have  now  kindly  asked  for  a new  edition. 

It  has  been  instructive  to  peruse  again  these  records  of 
earlier  experience  and  the  reflections  based  upon  them. 
Apart  from  a measure  of  discontent  with  the  style  and 
arrangement  of  certain  passages  I find  myself  approving,  on 
the  whole,  the  descriptive  and  critical  portions  of  the  book. 
The  clinical  portraiture  of  certain  diseases  and  their  course, 
which  it  was  my  main  object  to  provide,  together  with  the 
strong  plea  for  a maintenance  and  reinforcement  of  the  older 
disciplines  of  observational  medicine,  may  well  be  allowed 
to  stand.  Main  conclusions  and  recommendations  call  for 
no  drastic  revision.  The  ‘physician  as  naturalist’  remains 
a proper  ideal,  for  no  amount  of  scientific  training  or  tech- 
nical ability — and  wc  live  in  a highly  technical  age — can 
supply  those  qualities  of  naturalist  and  of  humanist  without 
which  the  good  physician  can  never  fully  earn  his  title. 

Where,  however,  I have  discussed  the  effects  of  thera- 
peutic measures  on  the  natural  progression  of  certain  infec- 
tions, several  chapters  have  fallen  badly  out  of  step.  The 
arrival  of  the  sulphonamides  and  penicillin  has  completely 
altered  the  course  and  prognosisof  the  streptococcal,  staphy- 
lococcal, and  pneumococcal  fevers  and  has  improved  the 
treatment  of  infections  with  Bacillus  colt.  Earlier  thera- 
peutic opinions  have  therefore  been  revised  in  several  places 
but,  since  treatment  is  considered  chiefly  in  its  relation  to 
course,  and  since  the  new  therapeutic  techniques  are  still  in 
process  of  development  and  my  own  experience  of  them  is 
very  limited,  I have  entered  into  no  detail.  I decided,  how- 
ever, to  leave  the  chapter  on  pneumonia  as  it  stood.  It 
would  be  a pity  if  the  student  were  to  lose  interest  in 


viii  PREFACE  TO  THE  SECOND  EDITION 

prognosis  and  in  the  difficult  judgements  which  it  requires, 
with  some  of  which  this  chapter  deals.  Just  as  the  twentieth- 
century  student  has  diminishing  opportunities  of ‘knowing’ 
syphilis,  so,  too,  will  lie  come  to  lose  his  chances  of  ‘know- 
ing’ the  pneumococcal,  meningococcal,  and  septic  fevers, 
which  he  combats  or  aborts  to-day  with  increasing  con- 
fidence. The  prognosis  of  pneumonia  at  all  ages,  and  even 
in  the  elderly,  has  already  been  greatly  changed.  Even 
pneumococcal  meningitis,  with  its  mortality  formerly  never 
far  from  100  per  cent.,  has  become  a more  curable  complica- 
tion with  the  aid  of  the  new  remedies.  The  long  and  painstak- 
ing trials  of  specific  sera  which  were  subjected  to  a critical 
review  in  Chapter  XIX  can  now  be  relegated  to  the  realm 
of  past  endeavour,  but  the  types  of  judgement  requisite  for 
assessing  new  methods  arc  the  same.  In  the  case  of  all  these 
grave  bacterial  infections  and  of  others  which  we  may 
shortly  learn  to  counter,  I should  like  to  enter  a plea  for 
better  attempts  in  future  to  arrive  at  more  reliable  statistical 
assessments  of  mortality  and  morbidity.  To  make  this  pos- 
sible much  better  standards  of  clinical  recording  will  be 
necessary.  Until  ‘cures’  can  be  computed  on  a statistical 
basis  we  cannot  form  precise  judgements  on  specific  or 
supposedly  specific  remedies.  Nor  should  we  ever  forget, 
for  all  our  new  skills,  that  Nature  is  still  ‘ the  physician  of 
diseases  \ 

The  sulphonamides  and  penicillin  in  many  hands  are 
being  wisely  used  and  often  with  appropriate  methods  of 
control.  In  many  others  they  are  being  employed  in  hap- 
hazard fashion,  almost  as  a panacea  for  unexplained  fevers 
and  for  symptoms  which  have  been  but  indifferently  under- 
stood. Clinical  medicine  is  brought  into  daily  disrepute  by 
such  neglect  of  basic  disciplines. 

As  a successor  to  Chapter  XIX,  I have  included  a new 
one  dealing  more  generally  with  the  uses  of  prognosis. 
Chapter  XXXII,  dealing  with  nosophobia — one  of  the  most 
widespread  of  all  diseases  but  often  undiagnosed  or  too 
lightly  regarded — -is  also  new. 

The  natural  history  of  disease  in  the  individual  is  still  the 
main  preoccupation  of  this  volume.  The  natural  history  of 


PREFACE  TO  THE  SECOND  EDITION  ix 

disease  in  the  community  is  a subject  at  least  as  worthy  of 
attention.  As  a reminder  of  the  importance  of  social  studies 
of  disease  and  of  some  of  the  methods  and  uses  of  what  may 
best  be  described  as  social  pathology,  I have  added  a single 
chapter  (Chapter  XXXVI)  bearing  upon  the  natural  history 
of  rheumatic  fever  in  this  country.  Social  pathology  has 
been  curiously  understressed — almost  to  the  point  of  neglect 
— in  the  teaching  of  the  text-books  and  the  schools,  but 
there  are  signs  now  of  awakening  interest  and  it  can  only  be 
a matter  of  time  before  this  branch  of  human  pathological 
inquiry  is  accorded  better  status  in  our  university  depart- 
ments. We  cannot  too  often  remind  ourselves  that,  in  the 
same  period  in  which  Addison,  Bright,  Gull,  and  Wilks  were 
laying  improved  foundations  to  human  medicine  and  the 
pathology  of  the  individual,  Chadwick  and  Farr  were  laying 
the  foundations  of  our  social  medicine  and  pathology — the 
former  by  his  great  surveys  and  the  close  correlations  of 
disease  with  poverty  and  squalor  which  he  revealed;  the 
latter  by  the  new  mathematical  precision  which  he  added 
to  socio-medical  investigation  and  the  power  which  he  im- 
parted to  the  dead  to  speak  on  behalf  of  living  and  unborn 
generations.  Outside  the  public  health  field,  bedside  patho- 
logy has  continued  to  absorb  the  attention  of  most  doctors 
to  the  exclusion  of  a parallel  interest  in  the  ultimate  and 
contributory  causes  and  social  consequences  of  all  the  more 
prevalent  diseases.  But  social  and  individual  pathology  are 
interdependent  sciences  and  prevention  is  still  more  impor- 
tant than  cure.  In  a more  socially  conscious  era  we  are 
beginning  to  move  forward  again  and  the  intimate  study 
of  health  and  sickness  and  their  aetiologies — in  families, 
schools,  occupational  groups,  and  larger  populations — will 
shortly  give  a new  impetus  to  academic  and  practical 
medicine.  Most  of  our  text-books  need  rewriting.  Students 
are  becoming  avid  for  information  and  for  types  of  experi- 
ence which  are  rarely  offered  them  in  the  hospital  ward  and 
the  laboratory. 

Numerous  small  corrections  have  been  made  to  the  text, 
but  the  general  character  of  the  original  chapters  remains 
unchanged. 


x PREFACE  TO  THE  SECOND  EDITION 

I am  indebted  to  the  Editor  of  the  Journal  of  the  Royal 
Sanitary  Institute  for  permission  to  incorporate  as  Chapter 
XXXVI  {with  some  additions  and  minor  modifications)  the 
substance  of  an  address  given  at  the  annual  conference  of 
the  Institute  at  Blackpool  in  I04G ; and  to  the  Editor  of  the 
Guy's  Hospital  Gazette  for  the  inclusion  (as  Chapter  XX) 
of  a modified  version  of  an  address  to  the  Pupils’  Physical 
Society  given  in  193S ; and  (as  Chapter  XXXII)  an  adapta- 
tion of  a clinical  lecture  given  in  1941. 

J.  A.  R. 

Oxford  1947 


PREFACE  TO  THE  FIRST  EDITION 

Of  the  thirty -four  papers  here  collected  the  majority  have 
appeared  previously  in  the  medical  journals  of  the  past  ten 
years  and  are  based  upon  addresses  to  medical  societies  or 
clinical  lectures  given  at  Guy’s  Hospital.  Their  concern  is 
with  subjects  of  general  medical  interest,  and  more  particu- 
larly with  symptomatology  and  the  portraiture  of  disease. 
They  are  to  be  regarded  as  gleanings  from  the  current  experi- 
ence of  a general  physican.  Other  occasional  essays,  bearing 
broadly  upon  the  natural  history  of  disease  or  the  methods 
and  ideals  of  its  students,  have  been  added. 

In  the  biological  sciences  as  a whole  experiment  and 
laboratory  observation  have  by  no  means  abolished  the 
necessity  for  field  work.  Indeed  the  importance  of  field  work 
is  being  more  than  ever  widely  acclaimed.  With  medical 
science  it  should  not  be  otherwise  and,  although  the  journals 
of  to-day  are  so  largely  occupied  with  the  results  of  bio- 
chemical, bio-physical,  and  bacteriological  research,  there 
is  still,  I believe,  ample  scope  and  genuine  need  for  plain 
clinical  description  and  discussion.  The  physician  is,  in  fact, 
and  will  remain  the  field-naturalist  of  those  numerous 
branches  of  human  biology  which  Medicine  comprises. 

With  this  for  justification,  my  decision  to  republish  these 
lectures  and  essays  in  book  form  is  further  due,  in  no  small 
part,  to  the  kindly  comments  which  several  of  them  have 
attracted  from  colleagues  in  this  country  and  the  United 
States  and  to  the  advice  of  friends.  I am  much  indebted  to 
the  editors  of  the  Guy's  Hospital  Reports , the  Lancet , the 
British  Medical  Journal,  the  Proceedings  of  the  Royal  Society 
of  Medicine,  t'ne  Practitioner,  the  CtinicaC  Journal,  and  the 
Guy's  Hospital  Gazette  for  their  permission  to  include  papers 
which  have  appeared  in  the  columns  of  their  journals. 
Dr.  R.  E.  Smith,  of  Rugby,  has  kindly  allowed  me  to  include 
my  portion  of  a paper  on  ‘Streptococcal  Fever*  which  we 
wrote  in  collaboration.  To  many  friends  in  practice  who 
have  given  me  the  opportunity  of  extending  my  experience 


xil  rHEFACE  TO  THE  FIRST  EDITION 

by  sharing  theirs,  and  to  my  old  teachers  and  my  fellow 
students  at  Guy’s,  I should  also  like  to  express  my  gratitude, 
for  their  inspiration  and  their  criticism  have  often  helped  me 
to  set  my  thoughts  in  order. 

Modifications  and  corrections  of  the  original  text  have 
been  necessary  here  and  there,  and  some  case-histories  have 
been  added  or  substituted  for  better  illustration  of  a theme. 
No  naturalist,  however  careful,  can  pretend  that  his  con- 
clusions arc  free  from  error,  but  I can  justly  say,  with 
William  Heberden,  that  ‘ the  notes,  from  which  the  follow- 
ing observations  were  collected,  were  taken  in  the  chambers 
of  the  sick,  from  themselves  or  from  their  attendants,  where 
several  things  might  occasion  the  omission  of  some  materia! 
circumstances ’,  and  that  I have  throughout  been  at  pains 
to  eliminate  ill-judged  hypothesis  and  to  avoid  undue 
reliance  upon  impressions  and  memories.  Full  notes,  fre- 
quently perused,  are  the  essence  of  clinical  education.  In 
the  keeping  of  my  case-notes  I have  been  blessed  with 
willing  and  expert  secretarial  aid,  for  which  my  thanks  arc 
due  to  Miss  Nora  McDonald.  In  the  betterment  both  of 
original  manuscript  and  proofs  I have  had  the  wise  nnd 
patient  assistance  of  my  wife. 


London 
January  1D3G 


J.  A.  It. 


CONTENTS 

I.  THE  PHYSICIAN  AS  NATURALIST  . . l 

II.  THE  TRAINING  AND  USE  OF  THE  SENSES  IN 

CLINICAL  WORK  . . . . .24 

III.  THE  CLINICAL  STUDY  OF  PAIN  . . .37 

IV.  VISCERAL  PAIN  AND  REFERRED  PAIN  . . 52 

V.  THE  STUDY  OF  SYMPTOMS  . . .CO 

VI.  THE  NATURE  AND  RELIEF  OF  SOME  COMMON 

GASTRIC  SYMPTOMS  . . .85 

Vn.  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER  03 
Vin.  ANOREXIA  . . . . .118 

IX.  CHRONIC  DIARRHOEA  . .130 

X.  FATTY  STOOLS  FROM  OBSTRUCTION  OF  THE 

I .ACTUALS  . . . . . .151 

XI.  OBSERVATIONS  ON  COLONIC  PAIN  . .161 

XII.  CHRONIC  SPASMODIC  AFFECTIONS  OF  THE 

COLON  AND  THE  DISEASES  WHICH  THEY 
SIMULATE .108 

XIII.  ON  EXAMINING  THE  RECTUM  . . .185 

XIV.  BALL- VALVE  ACCUMULATIONS  IN  THE  RECTUM  105 

XV.  VISCERAL  NEUROSES  . . . .201 

XVI.  THE  NATURAL  HISTORY.  PROGNOSIS,  AND 

TREATMENT  OF  STAPHYLOCOCCAL  FEVER  . 215 
XVn.  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 

TREATMENT  OF  STREPTOCOCCAL  FEVER  . 233 
XVin.  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
TREATMENT  OF  INFECTIONS  WITH  BACILLUS 
COLI  COMMUNIS  . . . . .251 

XIX.  THE  PROGNOSIS  AND  TREATMENT  OF  LOBAR 

PNEUMONIA  . . . . .265 

XX.  PROGNOSIS  . .....  278 

XXI.  THE  RADIAL  PULSE  . . . .295 

XXII.  HYPERPIESIA  . . . . .805 

XXIII.  CHRONIC  BRIGHT’S  DISEASE  WITHOUT  ALBU- 
MINURIA . . . . . .315 

XXIV.  ANGINA  PECTORIS  AND  ALLIED  SEIZURES  . 323 


xiv  CONTENTS 

XXV.  A NOTE  ON  JOHN  HUNTER’S  CARDIAC  INFARCT  S 


XXVI.  THREE  CASES  OF  CARDIAC  DISTRESS  . . S 

XXVII.  THROMBOPHLEBITIS  MIGRANS  . . .3 

XXVIII.  NOTES  ON  PROSTATIC  AND  CASTRIC  URAEMIA  3 
XXIX.  MYXOEDEMA  AND  OTHER  MANIFESTATIONS  OF 


THYROID  DEFICIENCY  . . . . 

XXX.  MENINGITIS  AND  MEXINGISM  . . . B‘ 

XXXI.  SOME  ALARMING  SEIZURES  . . . ® 

XXXII.  OF  NOSOPHOBIA  . . . . 3t 

XXXIII.  OBSERVATIONS  ON  THE  ABDOMINAL  AND 

CIRCULATORY  PHENOMENA  OF  ALLERGY  . 41 

XXXIV.  DIATHESIS.  OR  VARIATION  AND  DISEASE  IN 

MAN . , . . . . .4: 

XXXI'.  OPENING  REMARKS  AT  A DISCUSSION  ON  RE- 
SEARCH IN  CLINICAL  MEDICINE  . . « 

XXXVI.  THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  44 
XXXVII.  THE  HIPPOCRATIC  IDEAL  . . . .40 

INDEX  TO  AUTHORS  . . . . 4S 

SUBJECT  INDEX 43 


I 

THE  PHYSICIAN  AS  NATURALIST1 

In  that  part  of  his  discourse  on  The  Advancement  of  Learning 
which  concerns  the  work  of  the  physician,  Bacon  remarks, 
‘Only  there  is  one  thing  still  remaining,  which  is  of  more 
consequence  than  all  the  rest;  namely,  a true  and  active 
Natural  Philosophy  for  the  Science  of  Medicine  to  be  built 
upon.’  Ever  since  his  day,  with  the  genius  and  leadership 
of  great  minds  like  Harvey’s  and  Hunter’s,  with  discoveries 
due  to  experiment  in  the  hands  of  men  like  Jenner  and 
Lister,  with  steady  accumulations  of  knowledge  due  to  the 
observational  schools  of  Heberden,  of  Bright  and  Addison, 
of  Laennec  and  Trousseau,  and  the  contributions  of  the 
physiologists  and  pathologists,  our  profession  may  be  said 
to  have  been  laying  and  proving  those  foundations.  Should 
criticism  of  the  work  in  our  present  industrious,  if  less  illus- 
trious, age  be  asked,  it  would,  I think,  be  to  the  effect  that  in 
rearing  the  superstructure  we  incline  too  often  to  a neglect 
of  that  philosophy  which  has  provided  and  must  still  provide 
the  mortar  as  well  as  the  foundations  of  all  the  sciences. 

It  is  my  plan,  in  reviewing  some  functions  of  the  physi- 
cian, to  consider  especially  what  part  he  has  played  and 
may  continue  to  play  in  providing  the  bricks  and  mortar  of 
‘a  true  and  active  Natural  Philosophy’  in  medicine.  An 
‘active  philosophy’  we  may,  presumably,  take  to  mean  a 
progressive  one,  having  practical  bearings,  and  in  no  sense 
‘abstract '. 

Now  the  functions  of  the  physician  are  manifold.  There 
is  probably  no  servant  of  the  community  of  whom  a greater 
degree  of  omniscience  is  demanded,  or  upon  whom  a graver 
responsihifity  in  respect  of  personal  and  sometimes  social 
guidance  is,  from  time  to  time,  imposed.  As  a rule,  differing 
but  little  in  native  endowments  and  early  training  from 
others  who  are  given  the  advantages  of  a higher  education, 

1 An  address  given  to  the  Cambridge  University  Medical  Society,  29 
April  3931  (Guy's  JIosp,  Hep.,  1931,  Ixxxl.  278). 

B 


2 THE  PHYSICIAN  AS  NATURALIST 

he  is  nevertheless  expected  to  combine  in  his  person  the 
attributes  of  scientist,  healer,  priest,  and  prophet.  Fur- 
nished in  general  with  no  more  grey  matter  than  his  brothers 
in  other  professions,  he  is  yet  believed  by  many  of  his 
patients,  and  even  by  some  of  the  more  intelligent  among 
them,  to  have  the  key  to  secrets  unknowable  ns  well  as 
known.  It  is  almost  as  if  they  suspected  him  of  some  of 
the  magic  powers  of  the  ‘medicine  man’,  to  whom,  in  his 
guise  of  unqualified  or  qualified  ‘quack’,  they  are  only  too 
ready  to  fly  if  orthodox  endeavours  fail  to  convince  or 
cure  them. 

In  point  of  fact,  most  physicians  arc  no  more  than  good, 
honest  fellows  seeking  to  do  their  best  according  to  their 
lights,  in  an  arduous  profession  and  in  the  face  of  great 
difficulties,  by  a combination  of  humane  feeling  with  care- 
ful observation  and  common  sense  superimposed  upon  n 
background  of  scientific  education.  Although  the  two  may 
go  hand  in  hand,  the  physician's  material  success  is  by  no 
means  always  a measure  of  his  ability.  The  former  depends 
not  a little  upon  personality,  appearance,  and  powers  of 
persuasion.  The  latter,  as  I shall  hope  to  show,  is  a measure 
of  his  aptitude  and  training  as  an  observer  of  nature.  Skill 
in  diagnosis  and  prognosis  comes  only  with  careful  and 
continued  schooling  in  observation;  therapeutic  achieve- 
ment is  seldom  outstanding  unless  it  be  based  upon  accuracy 
in  diagnosis,  judgement  in  prognosis,  and  psychological  in- 
sight, for  all  of  which  a proper  understanding  of  the  natural 
history  of  disease  in  man  and  of  man  in  disease  is  a necessary 
equipment. 

In  taking  ‘the  physician  as  naturalist’  for  my  theme,  I 
am  therefore  electing  to  discuss  him  in  relation  to  what 
would  seem  to  be  his  most  essential  function. 

The  Mexsieo  oy  ‘ Physician’ 

Now  the  conception  of  the  physician  as  a naturalist  is  at 
least  as  old  as  Hippocrates,  the  first  among  physicians  and 
one  of  the  greatest  of  the  early  natural  philosophers.  With 
the  passage  of  time,  however,  the  name  lias  come  to  convey 
ideas  of  another  kind.  It  is  well  that  we  should  pause  occa- 


THE  PHYSICIAN  AS  NATURALIST  8 

sionally  to  consider  the  original  meaning  of  words  in  com* 
mon  use.  In  an  address1  given  in  1888  Professor  W.  T, 
Gairdner  of  Glasgow  (from  whom,  being  unable  to  invent 
a better,  I have  borrowed  my  title,  although  my  reflections 
on  the  subject  are  of  a different  sort),  reminded  his  audience 
that  the  word  physician  must  originally  have  implied  not  a 
healer,  but  a student  of  or  nature,  and  that  physic, 
which  we  now  think  of  as  meaning  a drug  or  a medicine, 
must  have  had  the  same  derivation.  On  the  basis  of  this 
derivation  he  made  it  his  opening  argument  that  it  should 
be  the  prerogative  of  the  physician  ‘ to  be  trained  and  exer- 
cised after  the  best  manner  and  according  to  the  most 
thorough  discipline  of  the  science  of  his  age;  and  that  he 
ought  to  be  (or,  at  least,  that  he  has  been  in  very  remote 
times)  regarded  as  being  admirable  and  trustworthy  as  a 
healer  or  physician,  chiefly  in  proportion  to  the  confidence 
reposed  in  him  as  a naturalist , that  is,  a humble,  reverent 
and  exact  follower  and  student  of  Nature  \a  To  this  argu- 
ment, although  specialization  and  other  developments  in 
our  profession  have  come  to  vary  the  equipment  and  calling 
of  its  individual  members,  we  should  all  subscribe. 

In  pursuit  of  my  programme  I shall  seek  to  compare  the 
spirit  and  functions  of  the  naturalist  with  the  spirit  and 
functions  of  the  physician ; to  consider  how  far  the  achieve- 
ments of  certain  great  physicians  in  the  past  have  depended 
upon  their  ability  as  naturalists;  to  remind  you  of  some 
among  them  who  were  recognized  also  as  good  natural 
historians  in  the  usual  sense  of  the  term ; and  to  insist  that 
the  training  and  ideals,  now  and  in  the  future,  for  all  that 
is  truly  physicianly  in  the  work  of  the  general  practitioner, 
the  consultant,  and  the  specialist,  are  just  the  same  training 
and  ideals  which  are  regarded  as  essential  for  the  develop- 
ment of  the  good  naturalist.  With  a brief  digression  on  the 
contributions  of  observation  and  experiment,  I shall  con- 
clude with  some  remarks  on  the  selection  and  training  of 
the  physician  and  on  the  manner  in  which  his  difficult 
course  may  best  be  laid. 

1 The  Physician  as  Naturalist,  Glasgow,  188$. 

* Op.  cit. 


TIIE  PHYSICIAN  AS  NATURALIST 


Tiie  Spirit  and  Functions  of  hie  Naturalist 

In  the  naturalist  we  behold,  or  so  it  seems  to  me,  the 
cultivation  and  ultimate  development  of  all  that  is  com- 
mendable in  the  native  inquisitiveness  of  childhood.  The 
young  of  Homo  sapiens,  when  wisely  handled  and  neither 
curbed  with  rebukes  nor  frustrated  with  lies,  commonly  ask 
the  most  searching  and  sensible  questions,  and  are  ever 
seeking  to  know  not  only  ‘What?’,  but  also  ‘How?  ' and 
‘Why?’.  They  are  often  acute  observers,  nnd  it  is  in  their 
desire  to  understand  natural  phenomena  that  wc  find  them 
most  avid  nnd  most  interesting.  But  alas,  when,  in  hap- 
pier circumstances,  wc  might  guide  him  in  his  natural  bent 
and  foster  an  embryo  Darwin,  hoary  custom  and  the  educa- 
tional systems  of  the  country’  snatch  our  child  away  to 
have  his  head  packed  with  instructions  and  book-lore  until, 
in  most  instances,  the  desire  to  know  by  observation  and 
experiment  is  crowded  out  and  his  feet  are  set  in  the  fixed 
pathways  of  a routine  or  official  life.  He  becomes  a business 
or  professional  man.  His  relief  from  drudgery*  is  found  in 
sport,  or  sometimes  in  literature  or  art.  He  loses  the  in- 
quiring faculty  and  ceases,  as  a rule,  to  ponder  the  entranc- 
ing problems  of  life  and  the  great  environment  of  life.  Our 
admiration  for  those  who  keep  and  foster  the  inquiring 
faculty  in  spite  of  the  toils  of  a stereotyped  schooling  should 
therefore  be  an  exalted  one.  Our  naturalists,  retaining  the 
clear-eyed  curiosity  of  youth,  both  feed  and  reward  it  with 
the  experience  and  wisdom  of  years.  For  ever  seeking  first- 
hand knowledge,  they  are  for  ever  refreshed  and  in  turn 
refresh  all  human  thought. 

Naturalists  are  of  many*  kinds  and  creeds,  but  they  hold 
certain  attributes  in  common,  and  notably  the  desire  to 
establish  the  truth  of  things  by  observing  and  recording, 
by  classification  and  analysis.  Some  of  them  are  in  a sense 
specialists  in  that  they  coniine  their  attentions  to  a single 
branch  of  natural  study,  and  that,  maybe,  a small  one. 
But  the  term  ‘naturalist*  is  employed  as  a rule  in  a wider 
sense,  and  the  naturalistic  temperament,  I believe,  forbids 
rigid  specialism.  Thus,  you  will  commonly  find  that  a man 


THE  PHYSICIAN  AS  NATURALIST  5 

widely  known  as  a specialist  in  one  branch  of  science  has, 
actually,  far  wider  interests.  A friend  of  mine,  chiefly  emi- 
nent in  the  field  of  morbid  histology,  in  his  spare  time 
earns  an  almost  equal  eminence  for  his  knowledge  of  beetles 
and  is  no  mean  botanist,  while  those  who  meet  him  in 
friendly  converse  and  read  his  papers  know  him  for  a student 
of  philosophy. 

Our  country  has  been  peculiarly  rich  in  naturalists.  Let 
us  take  three  examples — men  of  widely  varying  heart  and 
calibre,  but  all  to  be  counted  among  the  heroic  figures  of 
natural  philosophy.  Darwin  in  the  immensity  of  his  endea- 
vour and  the  majesty  of  his  thought  towers  above  the  rest. 
It  is  interesting,  and  in  support  of  my  contention,  that  his 
boyhood  education  was  altogether  a failure;  he  hated  being 
taught  and  could  not  learn  in  the  traditional  way.  Experi- 
ence was  his  sole  school.  He  observed,  he  collected,  he 
recorded,  and  he  deduced.  His  knowledge  extended  over 
fields  immeasurably  wide  and  applied  itself  to  details  infi- 
nitely small.  He  considered,  it  would  almost  seem,  every 
form  and  attribute  of  living  matter.  Had  medicine  not 
been  distasteful  to  him,  and  presumably  too  confined  a 
subject  and  too  set  about  with  unpleasing  interruptions  to 
thought,  he  might  have  become  the  greatest  physician  that 
ever  lived,  for  he  would  have  left  no  stone  unturned  in  his 
will  to  discover  everything  knowable  about  Man  in  health 
and  disease,  about  Man  in  relation  to  his  environment,  his 
ancestry,  and  to  his  natural  enemies  in  the  shape  of  sickness 
and  injury.  No  narrow  specialism  would  ever  have  applied 
its  blinkers  to  him.  He  would  have  embraced  anatomy, 
physiology,  pathology  and  psychology,  anthropology  and 
sociology  in  his  grasp,  dissecting,  assessing,  and  moulding 
them  and  learning  their  proper  places  in  that  whole  which 
we  call  Medicine.  Such  giants,  we  know,  are  rare  and  not 
to  be  emulated,  but  their  inspiration  is  gigantic  also  and 
abides. 

Huxley  was  another  giant  but  of  a different  kind.  He 
too  had  an  amazing  intellectual  grasp  and  clarity  of  vision, 
and  added  to  these  a fine.comhativeness.  We  know  him 
for  zoologist,  physiologist,  and  palaeontologist,  very  much 


C THE  PHYSICIAN  AS  NATURALIST 

a naturalist  and  in  no  sense  specialized.  A great  opponent 
of  dogma  and  tradition  in  education,  a staunch  advocate 
for  giving  the  natural  sciences  an  ever  more  prominent 
place  in  our  educational  system,  a fine  exponent  of  his  own 
knowledge  and  of  that  nequired  by  others,  and  possessed 
of  a literary'  ability  rare  in  scientists,  he  will  remain  for  all 
time  one  of  the  great  and  progressive  influences  in  natural- 
istic thought.  What  a fine  Professor  of  Medicine  he  would 
have  made!  How  he  would  have  rent  the  old  orthodoxies, 
and  forced  common  sense,  keen  observation,  and  the  im- 
portance of  cultivating  the  critical  faculty  on  his  students. 

And  next  let  us  take  Gilbert  White  of  Selhournc,  that 
peaceful,  parochial  sage,  watching  his  birds  and  his  seasons, 
his  flowers  and  his  weather-signals;  noting  all  down  in  his 
diaries  with  minute  care  as  to  time  and  dates;  observing 
behaviour  in  wild  things;  experimenting  with  echo  and 
dewponds ; tilting  at  superstitions ; and  handing  down  to  a 
grateful  posterity  his  homely  and  truthful  records.  Most 
fitly  did  a friend,  recognizing  the  wide  influence  his  Natural 
History  would  have,  write  to  congratulate  its  author  with 
the  remark  that  ‘it  will  correct  men’s  principles’.  Faithful 
observation  of  matters  of  fact  in  nature  must  ever,  in  a 
world  of  ignorance  and  prejudice,  serve  to  ‘correct  men’s 
principles’.  To  do  so  indeed  is  a main  function  of  the 
naturalist. 

If  Darwin  might  have  been  a greater  Hippocrates  and 
Huxley  the  greatest  Professor  in  Medicine,  Gilbert  White 
would  surely  have  supported  all  that  is  finest  in  the  his  tor)’ 
of  general  practice,  where  so  much  sound  learning  about 
disease,  about  man  in  conflict  with  his  environment,  about 
man  in  all  the  stages  of  his  individual  growth,  about  the 
inborn  and  extraneous  factors  in  disease,  and  about  the 
practical  handling  of  the  sick,  is  garnered.  Alas  that  so 
great  a part  of  it  should  pass  unsifted  to  the  grave  with  its 
tired  and  tried  discoverers. 

We  might  select  other  types  of  naturalist  for  comparison 
— -Linnaeus,  Waterton,  Yarrell,  Buckland,  Fabre,  or,  of 
more  recent  memory,  Hudson,  with  his  patience  and  strong 
sympathies  and  happy  gifts  of  style.  In  each,  I fancy,  we 


THE  PHYSICIAN  AS  NATURALIST  7 

should  discover  qualities  which  have  pertained  to  learned 
or  kindly  and  practical  physicians  through  the  ages.  The 
spirit  of  the  naturalist  is  the  spirit  of  science  combined  with 
that  of  philosophy;  it  seeks  to  ‘correct  men’s  principles’; 
to  enlarge  men’s  outlook;  to  pursue  and  teach  truth  for 
truth’s  sake;  to  increase  and  correlate  knowledge;  and  to 
make  what  is  remarkable  or  beautiful  in  nature  more 
interesting,  and  what  is  interesting  more  beautiful  or  re- 
markable. 

The  individualist  function  of  the  naturalist  is  to  satisfy 
his  own  intellect.  His  function  in  the  community  is  partly, 
indeed,  to  educate  and  inspire,  but  the  practical  applications 
of  his  work  in  man’s  affairs  are  also  to  be  regarded.  Gene- 
tics, stock-breeding,  forestry',  agriculture,  fisheries,  public 
health,  medicine,  and  psychology  are  in  debt  not  only  to 
the  Darwins  and  the  Huxleys,  but  to  an  army  of  humbler 
disciples  in  general  zoology,  botany,  entomology,  or  other 
branches  of  natural  knowledge. 

The  Spirit  and  Functions  of  the  Physician 

If  we  exclude  for  the  moment  (although  they  too  were 
essentially  naturalists)  the  great  discoverers  in  physiology 
like  Harvey  and  the  great  discoverers  in  the  realm  of  public 
health  like  Jenner,  both  of  whom  on  a basis  of  close  observa- 
tion evolved  an  historical  experiment,  we  find  that  the  ranks 
of  the  famous  physicians  are  chiefly  filled  with  men  belong- 
ing to  the  observational  school.  These  made  no  such  great 
revolution  in  thought  or  practice  as  did  Harvey  and  Jenner, 
but  they  provided  by  degrees  the  chapters  of  a great  un- 
compiled ‘Compendium  of  the  Natural  History  of  Disease’. 
Of  such  were  Hippocrates,  Sydenham,  Laennec,  Trousseau, 
Heberden,  Bright,  Addison,  Gull,  Wilks,  and  Osier.  Hippo- 
crates left  us  the  first  detailed  case-records,  studied  symp- 
toms and  the  influence  of  seasons,  and  wrote  a book  of 
remarkable  aphorisms  and  a system  of  prognostics.  Now 
prognosis  clearly  depends  upon  a knowledge  of  the  natural 
course  or  history  of  disease  and  of  the  manner  in  which  this 
is  influenced  by  age  and  sex  and  season  and  treatment; 
prognostic  ability  is  a special  mark  of  the  good  physician. 


8 THE  PHYSICIAN  AS  NATURALIST 

In  an  age  in  which  quacks  and  charlatans  abounded — not 
that  they  are  not  plentiful  to-day — he  insisted  on  an  under- 
standing of  the  nature  of  man  and  his  diseasesasancssential 
preliminary  to  any  therapeutic  system.  Of  his  observational 
ability  wc  have  repeated  records  in  Epidemics  and  in  the 
Aphorisms , wherein  he  describes  the  frothing  urine  of  ne- 
phritis and  the  ‘ curved  nails’  which  develop  in  empyema; 
and  records  the  bad  prognostic  significance  of  hiccup  in 
kidney  disease,  of  spasm  (tetanus)  following  wounds,  of 
speechlessness  and  stertor  in  apoplexy,  and  of  the  associa- 
tion of  a large,  hard  liver  with  jaundice,  and  so  forth.  Ilis 
experience  must  have  been  immense,  his  powers  of  observa- 
tion most  acute.  He  was  surely  a very  great  naturalist. 

Sydenham,  by  his  descriptions  of  fevers  and  gout,  and 
other  maladies,  faithfully  followed  the  Hippocratic  system. 
Pursuing  his  plan  of  ‘improving  physic’  by  ‘collecting  a 
genuine  and  natural  description  or  history  of  all  diseases 
as  can  be  procured’  he  earned  for  himself  the  title  of  ‘the 
English  Hippocrates’. 

Hcberden,  with  a clear  style  and  commendable  brevity, 
described  the  diseases  which  he  encountered  in  his  practice 
and  left  us  the  first  and  the  ablest  description  of  angina 
pectoris.  His  method  be  explains  in  the  preface  to  his  Com- 
mentaries on  the  History  and  Cure  of  Diseases  in  the  following 
words: 

•The  notes,  from  wliicb  the  following  observations  were  collected, 
were  taken  in  the  chambers  of  the  sick,  from  themselves  or  from 
their  attendants,  where  several  things  might  occasion  the  omission 
of  some  material  circumstances.  These  notes  were  rend  over  every 
month,  and  such  facts  as  tended  to  throw  any  light  upon  the  history 
of  a distemper,  or  the  effects  of  a remedy,  were  entered  under  the 
title  of  the  distemper  in  another  book,  from  wliich  were  extracted 
all  the  particulars  here  given,  relating  to  the  nature  and  cure  of 
diseases.’ 

You  will  remark  how  careful  he  is  to  dispense  with  the 
services  of  that  fickle  handmaid,  memory.  All  good  physi- 
cians and  naturalists  endeavour  to  take  their  notes  at  the 
time  of  their  observations,  in  order  to  possess  true  records 
for  comparison  and  analysis,  and  to  secure  accuracy  in 
anything  which  they  may  subsequently  write. 


THE  PHYSICIAN  AS  NATURALIST  0 

Bright  and  Addison,  the  two  great  physician-pathologists 
of  the  Guy’s  school,  combined  with  the  most  careful  study 
of  disease  in  man  an  equally  careful  examination  of  the 
body  after  death.  On  the  basis  of  their  case-records  they 
were  able  to  establish  the  identity  of  the  diseases  which 
have  been  named  after  them,  and  of  many  other  conditions 
since  clearly  recognized,  but  before  their  time  unfamiliar 
because  their  thorough  observational  methods  had  not  come 
into  vogue. 

If  we  read  the  lives  and  writings  of  these  great  physicians 
we  cannot  but  be  impressed  by  their  industry  and  their 
eager  spirit  of  inquiry,  which,  often  with  sacrifice  of  time 
and  health,  became  the  central  motive  of  their  lives,  the 
constant  claims  upon  their  professional  services  notwith- 
standing. The  spirit  which  actuated  them  was  the  same 
spirit  which  actuated  the  great  naturalists.  Their  function 
was  identical.  It  was  to  improve  knowledge,  to  ‘correct 
men’s  principles’.  If  in  the  process  it  often  happened  that 
the  principles  of  treatment  as  well  as  the  general  recognition 
of  disease  in  man  were  furthered,  their  social  utility  was 
only  the  more  enhanced. 

Now  you  may  object  that  I have  chosen  for  my  compari- 
sons only  the  more  eminent  among  the  naturalists  and  the 
physicians.  That  is  true.  I have  done  so  because  we  of  the 
rank  and  file  have  drawn  so  much  inspiration  from  them 
and  because  it  is  good  to  remember  indebtedness.  At  the 
same  time,  however,  and  in  the  same  way,  if  in  a lesser 
degree,  it  is  certain  that  all  other  naturalists  or  physicians 
worthy  of  the  name  have  subserved  and  will  continue  to 
subserve  these  functions,  moved  by  the  same  spirit  to 
render  their  contributions  to  human  knowledge. 

Physicians  who  were  also  Naturalists 
If  the  spirit  and  functions  of  the  naturalist  and  the 
physician  be  so  similar  it  would  not  be  surprising  to  dis- 
cover that  physicians  have  commonly  been  naturalists  in 
other  fields.  This  is  indeed  the  case.  Many  of  us  are  no 
doubt  acquainted  with  family  doctors  who  are  experts  in 
ornithology,  entomology,  or  botany  or  in  some  other  branch 


10  THE  PHYSICIAN  AS  NATURALIST 

of  natural  science.  If  you  should  have  the  chance  to 
peruse  the  earlier  volumes  of  the  Philosophical  Transac- 
tions of  the  Royal  Society  you  will  be  interested  to  note 
how  frequently  contributions  on  widely  various  scientific 
subjects  came  from  the  hands  of  medical  men.  If  you  ex- 
amine to-day  the  membership  lists  of  nny  big  society  such 
as  the  British  Ornithologists*  Union  or  of  any  local  natural 
history’  society  you  will  find,  I think,  that  the  medical 
profession  is  better  represented  than  any  other.  Although 
I have  no  such  records  before  me,  I can  assemble  at  once  to 
my  mind  a long  list  of  able  naturalists  among  my  colleagues 
in  general  and  consulting  practice.  There  are  also  notable 
examples  of  men  who  set  out  to  become  doctors  but  were 
soon  more  powerfully  attracted  to  other  fields  in  natural 
philosophy.  Darwin,  Huxley,  and  Buckland  were  among 
these. 

All  this  but  serves  to  show  that  the  naturalistic  tempera- 
ment and  the  physicianly  temperament  are,  as  we  should 
imagine,  close  relations,  if  not  identical  twins.  It  also  lends 
support  to  my  contention  that  the  physicianly  or  natural- 
istic temperament  is  expansive  and  out  of  accord  with 
specialism.  Although  other  examples  might  be  quoted,  I 
am  content  to  refer  to  two  great  physicians  only  who 
were  no  mean  naturalists  outside  their  professional  lives. 
Edward  Jenner,  the  discoverer  of  vaccination  and,  inci- 
dentally, the  first  to  associate  angina  pectoris  with  disease 
of  the  coronary  arteries,  published  a very  important  paper 
on  the  cuckoo  in  the  Philosophical  Transactions  for  1788. 
He  also  anticipated  Darwin  in  some  observations  on  the 
utility  of  earthworms,  and  was  very  helpful  in  furthering 
experiments  and  securing  specimens  for  John  Hunter,  who 
had  a great  regard  for  him.  In  one  of  his  letters  to  Jenner, 
Hunter,  then  engaged  upon  experiments  on  hibernating 
animals,  writes : * I own  I was  glad  when  I heard  you  was 
married  to  a woman  of  fortune ; but  “let  her  go,  never  mind 
her”.  I shall  employ  you  with  hedgehogs,  for  I do  not  know 
how  far  I may  trust  mine.* 

Richard  Bright,  before  he  settled  down  to  his  historic 
work  at  Guy’s,  had  accompanied  an  expedition  to  Iceland, 


THE  PHYSICIAN  AS  NATURALIST  11 

acting  as  zoologist  to  the  party,  and  later  contributing  notes 
on  botany  and  zoology  to  Mackenzie’s  Travels  in  Iceland. 
At  the  age  of  twenty-nine  he  produced  a remarkable  quarto 
volume  of  Travels  from  Venice  through  Lower  Hungary , in 
which  he  sets  out,  with  the  same  meticulous  care  and  the 
same  precision  in  observation  which  we  see  later  in  his 
medical  writings,  all  that  he  could  note  of  places  and  people, 
of  customs  and  dialects  and  the  general  conditions  of  life 
abroad  in  the  course  of  a long  and  none  too  comfortable 
journey.  It  is  interesting  to  compare  his  Travels  and 
a volume  of  his  beautifully  documented  and  illustrated 
Reports  on  Medical  Cases . 

The  Natural  History  of  Disease  in  Man 
It  might  be  supposed  that  the  natural  history  of  disease 
in  man  would  be  a main  concern  of  the  modern  physician 
just  as  it  was  a main  concern  of  Hippocrates  and  his  earlier 
disciples.  I am  doubtful  whether  this  supposition  could  be 
universally  supported  to-day.  Tempora  mutantur,  and  with 
them  the  scope  and  method  of  physicians.  It  becomes  neces- 
sary to  remind  ourselves  how  rapid  advances  in  learning 
may  sometimes  serve  to  make  the  principles  and  conduct 
of  a science  or  profession  more  rather  than  less  difficult. 
Discoveries  in  physiology,  biochemistry,  and  bacteriology 
and  the  constant  introduction  of  new  methods  of  clinical 
inquiry  have  so  far  added  to  the  burden  of  the  medical 
curriculum  and  complicated  the  training  and  the  work  of 
the  medical  man  that  it  has  become,  for  the  time  being, 
increasingly  hard  for  him  to  hold  the  scales  of  judgement 
and  to  maintain  what  Gull  called  ‘the  general  view’.  By 
the  demands  of  examining  bodies  the  student  spends  roughly 
two-thirds  of  his  time  "with  the  preliminary  and  ancillary 
sciences  and  one-third  only  with  patients.  He  embarks 
upon  this  latter  third  of  his  course  with  his  thoughts  rightly 
imbued  with  the  importance  of  experiment  and  of  labora- 
tory methods,  but  is  asked  of  a sudden  to  contemplate  the 
bewildering  problem  of  man  in  disease.  Even  in  the  wards 
he  is  often  encouraged  to  think  too  biochemically  or  radio- 
logically,  for  many  of  the  eases  there  are  problematical  and 


12  TIIE  PHYSICIAN  AS  NATURALIST 

admitted  for  special  investigations,  and  he  docs  not  see 
enough  of  disease  in  its  simpler  forms  and  early  stages  and 
in  its  natural  environments.  With  some  accidental  bias 
acquired  at  this  time  he  may  very  readily  come  to  think 
overmuch  in  terms  of  chemistry  or  bacteriology  or  surgery. 
It  is  at  first  wcllnigh  impossible  for  him  to  win  through  to 
that  point  of  vantage  from  which  medicine  can  be  regarded 
as  the  general  ‘biology  of  man  in  disease’,  and  not  as  a 
congeries  of  loosely  linked  sciences  and  specialisms  con- 
cerned with  parts  rather  than  wholes,  and  often  rather  with 
the  ‘seed’  than  with  the  ‘soil’,  which  is,  actually,  his  more 
immediate  concern.  At  no  point,  os  a rule,  is  he  offered  the 
strong  helping  hand  of  a broad  medical  philosophy.  No 
wonder  lie  is  sometimes  confused  or  even  disappointed,  and 
frequently  attracted  into  a service,  a laboratory,  or  a special- 
ism, wherein,  as  it  seems,  he  can  apply  himself  contentedly 
to  a limited  field  of  facts,  or  acquire  a technical  skill  which 
will  bring  him  bread  and  butter  and  a sufficiency  of  interest. 
How  is  he  to  acquire  the  ‘general  view’,  how  shall  he  learn 
to  become  more  of  a naturalist  and  less  of  a receptacle  for 
laboratory  loro  or  the  tenets  and  teachings  of  individual 
professors  ? 

I cannot  but  feel  that  of  late,  in  the  process  of  pursuing 
the  small  and  special  truths  which  relate  to  the  causes  and 
more  intimate  processes  of  disease,  we  have  as  a profession 
been  falling  into  the  error  of  neglecting  the  large  and  central 
truths  which  concern  the  nature  of  disease  itself.  It  is  clear 
that  the  word  disease  holds  very  different  definitions  for 
different  people.  For  the  patient  it  is,  in  a literal  sense,  liis 
dis-ease,  his  pain  or  breathlessness,  his  distress  of  body  or 
mind.  For  the  pathologist,  the  surgeon,  or  the  physician 
it  holds  other  interpretations.  Let  us  take  an  example.  A 
duodenal  ulcer  to  the  pathologist  is  a small  punched-out, 
circular  lesion  situated  just  distally  to  the  pyloric  sphincter, 
having  a smooth  edge  and  in  the  process  of  its  development 
destroying  one  or  more  coats  of  the  intestinal  wall.  Around 
it  he  visualizes  with  his  microscopic  eye  a thickened  sub- 
mucous layer  with  varying  stages  of  fibrosis.  To  the  sur- 
geon as  therapeutist  a duodenal  ulcer  is  apt  to  appear  as 


THE  PHYSICIAN  AS  NATURALIST  13 

a small  local  evil  to  be  excised  or  circumvented  with  skilful 
handicraft  and  recorded  as  another  ‘conquest’,  with  the 
happy  sequel  of  a patient  sent  on  his  way  rejoicing — unless 
he  be  among  those  unfortunates  who  suffer  a relapse.  The 
physician  as  naturalist  can  take  no  such  restricted  view  as 
either  of  these.  He  thinks  of  ‘duodenal  ulcer’  in  terms  of 
a peculiar  and  interesting  type  of  hunger-pain  of  rhythmical 
periodicity,  associated  with  the  local  condition  which  the 
pathologist  describes,  afflicting  persons  of  particular  physi- 
cal and  psychological  types,  occurring  five  times  as  fre- 
quently in  men  as  in  women,  showing  a definite  familial 
tendency  and  a pronounced  seasonal  fluctuation,  and  carry- 
ing with  it  liabilities  in  respect  of  haemorrhage,  perforation, 
scarring,  or  intermittent  disability  from  a wearisome  dys- 
pepsia. He  is  aware  that  it  has  at  first  a natural  tendency 
to  self-healing  and  that  in  its  earlier  stages  such  healing  can, 
under  suitable  conditions  of  dietary  and  physiological  rest, 
be  encouraged  and  consummated  for  long  periods  or  even 
through  life.  In  later  stages  the  tendency  to  relapse  in  spite 
of  treatment  increases.  As  a physiologist  he  appreciates  its 
common  association  with  a native  hyperchlorhydria  and 
the  high,  short  stomach  which  the  radiologist  reveals.  His 
studies  incline  him  to  the  view  that  focal  infections  and 
nicotine,  but  perhaps  still  more  the  mental  and  physical 
fret  and  stress  of  civilized  city-life,  contribute  to  the  per- 
petuation, if  not  to  the  actual  causation,  of  the  disease.  He 
knows  that  without  knowledge  of  this  kind  his  treatment 
and  prognosis  in  individual  cases,  and  his  decision  as  be- 
tween a medical  or  a combined  surgical  and  medical  cam- 
paign of  treatment,  would  be  ill  judged  and  insecure.  He 
endeavours  to  study  the  disease  from  every  possible  angle, 
as  an  ornithologist  might  study  the  morphology,  the  habits, 
and  the  environment  of  a bird.  By  information  so  gathered, 
information  which  the  particular  teaching  of  pathology,  bio- 
chemistry* surgery,  or  radiology,  whether  severally  or  in 
concert,  could  never  give,  he  gradually  establishes  his  claim 
to  an  understanding  of  duodenal  ulcer  in  man,  and  of  man 
afflicted  with  duodenal  ulcer,  as  reasonable  and  complete 
as  present  conditions  will  allow. 


14  THE  PHYSICIAN  AS  NATURALIST 

Or  take  some  wholly  different  malady  like  pneumonia. 
The  laboratory-man  may  think  of  it  in  terms  of  ‘anti- 
bodies’ and  varying  types  of  pneumococcus,  and  if  he 
dabbles  in  therapeutics  may  hold  himself  justified  in  pre- 
scribing treatment  with  vaccine  or  scrum.  The  physician 
knows  that  at  certain  ages  and  in  certain  patients  the 
disease  will  run  a particular  course  to  spontaneous  recovery 
within  a certain  brief  time,  and  that  in  such  case  it  would 
be  wholly  unwise  to  experiment  with  medicines,  vaccines, 
or  sera.  In  children  after  the  first  year  or  two  lobar  pneu- 
monia is  particularly  benign.  In  adult  life  there  is  a much 
less  certain  outlook,  and  there  is  a mortality  which  vnries 
with  season,  with  country,  and  with  epidemic,  all  factors 
which  make  it  extremely  difficult  to  form  judgements  about 
the  efficacy  of  remedies.  Certain  conditions,  such  as  alcohol- 
ism, greatly  raise  the  mortality  of  pneumonia.  In  individual 
cases  there  are  symptoms  and  signs  which  compel  a hopeful, 
a guarded,  or  a pessimistic  outlook.  Knowledge  of  this  kind, 
with  its  intimate  bearing  on  the  conduct  of  cases,  can  only 
come  through  prolonged  study  of  the  disease  in  man.  Ani- 
mal studies  and  bacteriology  may  be  helpful,  but  they  are 
often  misleading. 

It  now  becomes  pertinent  to  return  to  our  question  in 
regard  to  the  nature  and  definition  of  a disease.  Clearly  it 
is  not  merely  a symptom  or  a group  of  symptoms ; it  is  not 
the  local  injury  nor  the  general  poisoning  which  gives  rise 
to  the  symptoms;  nor  yet  the  bacteria!  invasion  which 
gives  rise  to  the  injury  (or  the  poisoning)  which  causes  the 
symptoms.  Might  we  not  define  a disease  as  'the  it  hole 
consequence  of  a conflict  between  man  (or  animal)  and  the 
noxious  agencies  in  his  environment'  ? This  includes  the 
concept  of  ‘soil’  as  well  as  ‘seed’,  and  indeed  of  all  the 
intrinsic  and  extrinsic  factors  at  work.  Sydenham  said,  ‘A 
disease,  in  my  opinion,  how  prejudicial  soever  its  causes 
may  be  to  the  body,  is  no  more  than  a vigorous  effort  of 
nature  to  throw  off  the  morbific  matter,  and  thus  recover 
the  patient.’  It  is,  in  other  words,  just  as  much  a natural 
phenomenon  as  health  or  as  man  himself,  its  victim,  are 
natural  phenomena,  and  as  such  it  should  be  studied. 


THE  PHYSICIAN  AS  NATURALIST  25 

Pneumonia  or  any  other  disease  in  an  individual  may  be 
influenced  in  its  course,  not  only  by  the  type  of  the  invading 
microbe,  but  also  by  the  age  and  type  of  the  patient,  by 
his  hereditary  endowments,  by  his  environment  and  his 
psychology,  and  even,  as  Hippocrates  knew,  by  the  psycho- 
logy of  his  attendants.  Unless  we  can  appreciate  all  this  we 
are  not  good  naturalists  and  we  are  not  in  a position  to 
diagnose  (or  ‘thoroughly  know’),  to  ‘prognose'  (or  fore- 
cast), and  to  treat  as  ably  as  we  might  do.  A knowledge  of 
the  natural  history  of  disease  is  essential  in  therapeutics. 
Gull  and  Sutton1  studied  the  natural  history  of  rheumatic 
fever  by  treating  a series  of  cases  with  mint- water,  and  were 
thereby  able  to  show  that  certain  remedies  then  advocated 
had  no  appreciable  influence  on  its  course  or  behaviour. 
From  time  to  time  ‘cures’  for  problematical  diseases  like 
disseminated  sclerosis  are  announced  by  physicians  who 
have  not  been  at  pains  to  familiarize  themselves  with  the 
long  remissions  and  psychological  reactions  peculiar  to  the 
malady. 

Diseases,  like  races,  vary  in  character  at  different  times 
and  in  different  places.  They  may,  like  races,  under  varying 
conditions,  appear  and  disappear,  as  we  have  witnessed  in 
the  case  of  chlorosis.  These  features  in  their  history  are  also 
worthy  of  attention. 

The  Natural  History  or  Man  in  Disease 

Perhaps  I have,  already  made  the  study  of  disease  appear 
too  vast  and  difficult  for  you  by  insisting  on  the  value  of 
what  Smuts2  would  call  the  holistic  view  (from  oAoj  = whole). 
In  point  of  fact,  and  given  a reasonable  interest  in  one’s 
fellow  men,  this  is  really  a simpler  doctrine  than  that 
which  is  commonly  offered  to  the  medical  student  in  the 
later  clinical  period  of  his  training.  Here  he  is  confronted, 
at  what  should  be  the  summit  and  summary  of  his  pre- 
graduate education,  with  a loosely  connected  series  of 

1 A Collection  of  the  Published  Writings  of  Sir  William  Gull,  New  Syden- 
ham Society,  1894. 

* Holism  and  Evolution,  by  General  the  Rt.  Hon.  J.  C.  Smuts,  Macmillan, 
London,  1927. 


10  THE  PHYSICIAN  AS  NATURALIST 

special  studies,  which  have  lost  touch  with  physiology, 
which  separate  part  from  part,  and  cause  from  effect,  and 
give  him,  ns  a rule,  but  little  clue  as  to  what  are  essentials 
and  what  non-essentials  in  human  medicine;  which  find 
their  material  altogether  too  much  among  the  ‘end-result’ 
diseases  of  the  hospital  ward;  and  which  have  for  their 
aim  not  so  much  a reasoned  understanding  of  common 
problems  ns  the  satisfaction  of  individual  teachers  and  the 
passing  of  examinations. 

I have  postulated  a ‘reasonable  interest  in  one’s  fellow 
men'  ns  necessary  for  the  holistic  or  naturalistic  view  of 
disease,  for  the  proper  study  of  mankind,  whether  sick  or 
well,  is  surely  man.  lie  is  the  instrument  whereby  wc  study 
his  diseases  and,  unless  we  know  the  varying  temper  of  the 
glass,  the  delicacy  of  the  gauges,  and  the  mechanisms  under 
the  set  experiments  of  health,  wc  shall  not  rightly  follow  the 
processes  of  those  experiments  of  Nature’s  which  we  call 
disease.  Laboratory  physiology  can  only  tell  us  a tithe  of 
the  health-experiment.  We  have  need  of  a broader  and 
more  observational  human  physiology,  more  cognisant  of 
human  variety.  Every  man  is  endowed  at  birth  by  his 
parents  and  ancestors  with  a type  of  constitution  built  of 
anatomical,  physiological,  immunological,  and  psychological 
material  which  will  help  to  determine  his  course  through 
life  and  his  reactions  to  environmental  stress  or  injur y. 
With  the  aid  of  family  histories  and  observations  of  physical 
and  mental  types  we  may  learn  to  recognize  or  predict 
certain  liabilities  in  the  way  of  disease.  Gout,  asthma,  per- 
nicious anaemia,  migraine,  epilepsy,  and  tuberculosis  all 
depend  in  some  degree  upon  such  constitutional  variations, 
which  are  quite  comparable  with  other  biological  variations, 
and,  like  them,  transmissible,  and  which  in  medicine  are 
sometimes  called  diatheses.  But  apart  from  these  special 
and  broader  variations  we  quickly  learn  that  every’  indivi- 
dual reacts  a little  differently  from  every’  other  individual 
to  adverse  as  well  as  to  beneficent  physical  and  psychic 
stimuli,  or,  in  the  old  phrase,  that  ‘one  man’s  meat  is 
another  man’s  poison*.  For  this  reason  the  physician  must 
ever  be  developing  his  understanding  of  human  types  and 


THE  PHYSICIAN  AS  NATURALIST  17 

reactions.  Until  he  attains  a certain  proficiency  in  this  he 
meets  with  many  pitfalls  and  handicaps.  His  task  is  not 
easy,  and  yet  you  shall  prove  for  yourselves  how  the  mani- 
fold things  to  be  observed  (whether  on  the  large  scale  or 
minutiae)  and  how  constant  practice  in  the  method  con- 
tinually maintain  the  fascination  of  his  work,  in  the  conduct 
of  which  he  can  scarcely  fail  to  experience  the  same  zest 
and  the  same  rewards  which  the  naturalist  in  other  fields 
experiences.  Eye  and  ear  and  hand  and  sense  of  smell  must 
be  trained  to  gauge  the  physical  divergencies  from  the 
normal  and  the  wide  variations  within  the  'normal'.  So, 
too,  the  mind  may  learn  to  watch  and  gauge  the  effects  of 
psychology  on  disease  and  of  disease  on  psychology.  The 
assessments  can  rarely  be  quantitative,  as  in  the  case  of 
your  physical  and  chemical  tests,  and  yet  experience  and  a 
grouping  of  rough  assessments  between  them  will  often  lead 
to  a high  degree  of  accuracy  in  the  final  opinion.  In  chronic 
renal  disease,  for  instance,  a very  close  estimate  of  the  de- 
gree to  which  the  blood-urea  has  been  raised  may  sometimes 
be  accomplished  by  experience  and  bedside  methods  alone, 
and  prognosis  can  be  determined,  as  a rule,  as  accurately 
by  these  as  by  any  combination  of  chemical  tests.  People 
sometimes  talk  of  the  physician’s  ‘intuition’  or  'clinical 
sense’.  There  is  no  such  thing,  unless  we  mean  by  the  terms 
quick  perception,  quick  memory,  and  quick  piecing  together 
and  application  to  a present  problem  of  past  experiences. 
All  the  senses  are  the  physician’s  weapons,  but  a good  visual 
memory  and  a lively  sympathy  are  his  best  allies.  Like  the 
modern  naturalist,  he  must,  metaphorically  speaking,  be 
ready  to  use  his  camera  and  his  ‘hide*  as  well  as  his  eyes 
and  his  note-book.  The  embarrassed  patient,  like  the  wild 
bird,  cannot  be  successfully  studied  if  he  is  self-conscious 
or  afraid. 


Observation  and  Experisient 
Discussion  in  the  journals  has  lately  centred  around  the 
question  of  the  relative  importance  to  medical  science  of 
observation  and  experiment.  Certain  sciences,  such  as 
chemistry,  physics,  and  modem  physiology,  are  essentially 


18 


TIIE  MIYSICIAN  AS  NATURALIST 
experimental.  Others,  like  zoology  and  astronomy,  are  ob- 
servational. In  the  biological  sciences  as  a whole  it  would 
seem  that  we  can  dispense  with  neither  method,  but  that 
experiment  in  the  future  is  likely  to  play  a much  larger  part 
than  heretofore.  In  psycholog}',  for  instance,  which  has 
been  so  largely  an  observational  study,  the  experiments  of 
Pavlov  on  conditioned  reflexes  have  come  to  modify  and 
stimulate  ideas.  Clinical  science  is  essentially  observational, 
and  the  present  scope  of  human  experiment  is,  for  obvious 
reasons,  small.  Nevertheless,  Sir  Thomas  Lewis1  believes 
that  future  progress  in  medicine  must  largely  depend  on  the 
application  of  experimental  methods  to  man  in  disease. 
With  his  contention  that  there  is  room  for  whole- time  and 
adequately  remunerated  research  appointments  in  clinical 
medicine  to  further  this  project  I am  in  full  agreement.  It 
is  well,  however,  to  remember  that  nearly  all  experiments 
have  developed  on  the  basis  of  earlier,  painstaking  observa- 
tions of  natural  phenomena,  and  that  there  is  actually  no 
great  dividing  gulf  between  the  two  methods.  As  Huxley 
put  it,  experiment  is  only  'artificial  observation The  ‘ob- 
server’ uses  the  slow,  vast,  and  difficult  experiments  of 
nature.  The  ‘experimenter’  creates  in’s  own  conditions  and 
is  thereby  able  in  a shorter  space  of  time  and  with  greater 
precision  to  obtain  the  necessary  proofs  for  the  establish- 
ment, to  his  satisfaction,  of  laws  and  principles  in  operation 
in  nature.  It  is  generally  allowed  that  many  of  the  most 
useful  discoveries  in  science  have  come  through  experiment. 
Harvey’s  discovery  of  the  circulation,  Jenner’s  vaccination, 
and,  more  recently,  Banting’s  discovery  of  insulin  are  note- 
worthy examples.  Darwin  and  Hunter  relied  far  more  upon 
extended  observation,  but  all  of  these,  in  point  of  fact,  were 
at  one  time  and  another  both  observers  and  experimenters. 

Briefly  there  can  be  no  dispute  about  the  merits  of  the 
two  methods;  they  are  complementary.  Experiment  is  the 
offspring  and  pupil  of  observation  and  may  in  time  achieve 
more  than  its  parent,  but  in  biology,  and  in  the  biology  of 
man  in  particular,  it  can  never  supersede  or  become  inde- 
pendent of  its  parent. 

1 Brit.  Med.  Joum.,  15  March  1930. 


THE  PHYSICIAN  AS  NATURALIST  10 

Those  of  you  who  are  attracted  to  experimental  science, 
as  I sincerely  hope  some  will  be,  would  do  well  to  remember 
that  observational  science  provides  a good  training-school, 
and  that  without  it,  in  medicine,  the  ideas  upon  which  most 
useful  experiments  are  based  would  not  be  born  at  all.  You 
are  quite  rightly  training  yourselves  and  being  trained  now 
in  the  more  exact  methods  of  physiology.  Shortly  you  will 
be  asked  to  acquire  the  observational  outlook  in  the  wards 
of  a London  Hospital.  You  will  naturally  try  to  apply  there 
the  knowledge  and  principles  which  you  have  acquired  here, 
and  at  first  it  may  seem  difficult,  for  the  problems  are  varied 
and  complex.  When,  however,  with  a growing  capacity  for 
observation,  you  begin  to  correlate  bedside  findings  and  the 
everyday  symptoms  of  disease  with  physiological  and  patho- 
logical knowledge,  then  indeed  medicine  will  become  for 
you  an  earnest  adventure  and  a delight  to  the  mind.  Then 
too  you  may  claim  that  the  holistic  or  naturalistic  philosophy 
is  beginning  to  display  its  harmonizing  influence. 

Most  of  you  are  destined  for  practice,  and  observation 
will  be  your  chief  standby,  but  it  would  be  a poor  thing  if 
you  had  not  also  been  given  an  experimental  training  and 
the  understanding  of  deeper  and  more  intimate  processes 
based  thereon.  Some  of  you  will  go  back  to  the  life  of 
experimental  research,  but  you  will  go  the  richer  for  having 
seen  the  problems  which  Nature  sets  us,  and  I would  urge 
you  not  to  be  in  too  great  a hurry  to  return  to  the  micro- 
scope or  the  test-tube  and  to  forget  the  fuller,  if  often  more 
baffling,  life  of  the  clinic,  the  out-patient  department,  and 
the  post-mortem  room. 

The  Selection  and  Training  of  the  Physician 
In  placing  before  you  the  claims  of  general  medicine  I 
may  at  times  seem  to  have  spoken  in  a disparaging  way  of 
specialism,  but  I would  not  for  a moment  have  you  suppose 
that  I regard  specialism  or  specialists  as  unnecessary.  Far 
from  it.  The  field  of  knowledge  is  altogether  too  vast  to 
be  explored  without  the  constant  aid  of  more  and  better 
specialism.  In  medicine  both  laboratory  and  clinical  special- 
ism have  made  far-reaching  contributions,  and  this  particu- 


20  THE  PHYSICIAN  AS  NATURALIST 

!arly  in  the  last  few  decades.  In  practice  we  arc  in  constant 
debt  to  specialist  colleagues  for  the  help  and  instruction 
which  they  give  us.  But,  without  n doubt,  there  can  be  too 
much  specialism,  and  over-specialism,  and  a neglect  of  co- 
ordination and  of  what  Bacon  called  ‘universality’,  and 
Smuts  would  call  ‘wholes’;  and  this  neglect,  I believe, 
obtains  at  present,  not  only  in  our  own  profession  but  in 
the  scientific  world  at  large.1  And,  in  common  with  many 
others,  I must  also  maintain  that  there  is  real  danger  in 
specializing  too  young,  before  the  intellect  is  proved  and 
fit,  and  that  we  may  and  do  behold  around  us  already  a 
breed  arising  which  lacks  much  of  what  was  admirable  in 
the  old  physicians  who  were  their  own  specialists,  and  much 
that  is  admirable  in  the  abler  specialists  who  arc  their  own 
physicians.  Among  a group  of  honoured  teachers  I have 
been  particularly  grateful  to  two — the  first  a surgeon,  and 
incidentally  a Doctor  of  Medicine,  with  ns  keen  an  interest 
in  the  medical  and  pathological  aspects  of  his  surgical  eases 
as  any  physician  or  pathologist  could  boast ; the  second  a 
physician,  a Fellow  of  both  the  Royal  Colleges,  who  con- 
stantly taught  by  example  the  importance  of  ' the  general 
view’  and  of  close  care  and  thoroughness  in  the  routine 
examination  of  cases.  And  surely  it  is  proper  that  eveiy 
specialist,  whether  medical  or  surgical,  should  retain  quali- 
ties appropriate  to  the  naturalist  or  physician.  You  may, 
it  is  evident,  require  devoted  application  and  long  practice 
to  become  on  able  cardiologist  or  aural  surgeon,  but  in 
neither  case  can  you  afford  to  confine  yourself  too  closely 
to  ‘ the  part*  or  to  neglect  that  ‘whole’  which  includes  both 

1 Bacon  (Advancement  of  Learning)  has  a very  concise  commentary  on 
‘specialism’  and  ‘holism’.  ‘Another  error ...  Is  the  over  early  and  peremp- 
tory reduction  of  knowledge  into  arts  and  methods;  from  which  time  com- 
monly sciences  receive  small  or  no  augmentation.  IJut  as  joung  men, 
when  they  knit  and  shape  perfectly,  do  seldom  grow  to  a further  stature; 
so  knowledge,  while  it  is  )n  aphorisms  end  observation*,  it  is  in  growth; 
but  when  it  once  Is  comprehended  in  exact  methods,  it  may  perchance  be 
further  polished  and  illustrate  and  accommodated  for  use  and  practice; 
but  it  Increaseth  no  more  in  bulk  and  substance.’ 

‘Another  error,  which  doth  succeed  that  which  we  last  mentioned,  is  that 
after  the  distribution  of  particular  arts  and  sciences,  men  have  abandoned 
universality,  or  phitosophia  primal  which  cannot  but  cease  and  stop  all 
progression.’ 


THE  PHYSICIAN  AS  NATURALIST  21 

your  patient  and  the  wider  fields  of  human  and  medical 
experience.  Conversely,  the  general  physician  and  the 
general  practitioner  can  never  afford  to  neglect  the  contribu- 
tions of  specialism.  They  should  never  presume,  and,  indeed, 
they  are  generally  far  too  humble  to  presume,  the  possession 
of  a medical  omniscience. 

Some  minds  clearly  prefer  to  seek  a more  perfect  efficiency 
in  a smaller  field.  The  physician  as  naturalist  prefers  the 
broader  study  of  man  in  disease,  and  in  the  process  is  ever 
grateful  for  the  additional  knowledge  which  comes  to  him 
through  the  specialist.  There  is  a facetious  definition  which 
states  that  the  specialist  is  4 one  who  knows  more  and  more 
about  less  and  less  ’,  and  the  dilettante  * one  who  knows  less 
and  less  about  more  and  more’.  I would  suggest  that  it  is 
the  proper  endeavour  of  physicians  and  naturalists  to  know 
‘more  and  more  about  more  and  more’.  Is  the  ambition 
too  presumptuous?  I believe  not,  if  the  task  is  entered 
upon  with  method  and  humility.  Not  all  minds  are  suited 
to  the  task ; and  no  more  are  all  minds  suited  to  a life  of 
experimental  research  or  clinical  specialism. 

It  is  just  here,  it  seems  to  me,  that  those  who  have  the 
privilege  for  a period  to  be  your  teachers  might  sometimes 
do  more  to  help  you  in  the  selection  of  your  careers,  by  dint 
of  knowing  your  earlier  inclinations  and,  when  possible, 
more  of  your  individual  characters  and  tastes,  being  less 
persuaded  than  is  commonly  the  case  by  the  claims  of  their 
own  departments.  Informed  as  to  your  ‘diatheses’,  they 
should  be  the  better  able  to  prognosticate.  The  man  of 
action,  ingenuity,  and  manual  dexterity  has  generally  shown 
signs  of  these  attributes  in  early  youth ; he  might  well  be 
advised  (if  he  will  but  remember  to  be  something  of  a physi- 
cian too)  to  think  of  surgery  or  a surgical  specialism.  The 
devotee  of  the  microscope  or  the  laboratory  bench  will  prob- 
ably be  happier  in  pathology,  bacteriology,  or  biochemistry 
and,  even  if  his  father  wants  him  to  join  him  in  the  practice, 
should  consider  the  alternative  life.  But  if  it  were  told  me 
of  another  that  he  had  from  boyhood  been  interested  in 
birds  and  beasts,  or  fossils  or  flowers ; that  he  kept  note- 
books of  his  observations  or  made  careful  collections  of 


22  TILE  PHYSICIAN  AS  NATURALIST 

specimens;  and  that  he  was  thoughtfully  and  widely  in- 
formed in  natural  lore — then  I should  strongly  advise  him 
(if  able  to  resist  the  call  of  country  practice)  to  think  of  the 
physician’s  life  as  his  destiny.  I should  know  that  he  would 
never  ‘apply  the  blinkers’,  that  his  naturalist’s  sense  would 
serve  him  in  good  stead,  that  he  would  continue  to  observe, 
record,  and  analyse  the  phenomena  encountered  at  the  bed- 
side and  in  the  consulting-room,  and  that  he  would  in  all 
probability  make  his  own  useful  contributions  to  the  study 
of  disease. 

And  what  of  his  training?  In  hospital,  and  later  with  his 
necessary  examinations  behind  him,  he  should  seek  contact 
with  patients  whenever  and  wherever  he  can,  given  only 
that  he  has  the  sense  to  avoid  ill  health  and  mental  weari- 
ness through  excess  of  routine.  He  should  attend  and  per- 
form as  many  post-mortem  examinations  as  possible.  lie 
may  have  to  wait  some  time  for  practice,  but  when  it  comes 
he  will  find  that  he  learns  more  from  his  private  patients  on 
the  whole,  if  he  keeps  a card-index  and  good  notes,  than 
form  his  hospital  cases.  His  case-books  or  files  will  be  his 
‘cabinets’,  his  good  diagnoses  (I  employ  the  term  in  its 
fullest  sense)  his  ‘naturalist’s  finds’.  At  frequent  intervals 
by  re-reading  and  analysing  his  notes,  after  the  manner 
suggested  by  Heberden,  and  sometimes  by  the  writing  of 
papers  he  should  seek  to  discover  how  far  his  first-hand 
knowledge  of  disease  has  advanced.  There  is  no  disease  of 
which  a fuller  or  additional  description  does  not  remain  to  be 
written:  there  is  no  symptom  as  yet  adequately  explored.  He 
should  meet  colleagues  in  all  branches  of  the  profession  as 
much  as  may  be,  and  picking  what  is  likely  to  prove  profit- 
able among  them,  should  attend  the  discussions  of  medical 
societies.  If  finance  and  opportunity  permit  he  should  also 
visit  foreign  clinics,  but  rather  as  a refreshment  and  with 
a view  to  seeing  others  at  work  and  learning  new  methods 
than  as  an  alternative  to  self-instruction.  In  addition  to 
the  practice  of  ear  and  eye  and  hand  the  practice  of  reason 
and  judgement  must  be  assiduously  cultivated.  We  roust, 

I fear,  confess  that  sound  logic  is  an  all  too  rare  display  in 
medical  writings  and  discussions.  He  should  endeavour  to 


THE  PHYSICIAN  AS  NATURALIST  23 

preserve  a just  balance  in  his  assessments  as  between  the 
physical  and  the  psychological,  and  the  constitutional  and 
the  environmental  factors  in  the  causation  of  his  patients’ 
maladies.  He  should  read  current  medical  literature  criti- 
cally and  the  old  masters  with  reverence.  He  should  not 
deny  himself  that  ‘leisure’  which  Hippocrates  regarded  as 
one  of  the  essentials  in  the  life  of  the  physician,  although 
he  may  find  it  hard  indeed  to  win.  A general  interest  in  the 
progress  of  biology  will  keep  him  stimulated  and  alert.  At 
times  he  will  be  weary  and  overworked,  at  times  very  wor- 
ried ; it  is  not  likely  that  any  excess  of  material  benefits  will 
come  his  way;  but  his  life  will  be  happy,  for  he  will  keep 
faith  with  his  intellect  and  his  calling  and  contribute  his 
mite  towards  the  foundation  of  ‘a  true  and  active  Natural 
Philosophy  * in  medicine. 


II 


THE  TRAINING  AND  USE  OF  THE  SENSES  IN 
CLINICAL  WORK1 

One  summer  afternoon  I was  conversing  with  an  old  Guy’s 
friend  in  his  garden  on  the  subject  of  plant-scents,  a subject 
to  which  he  has  devoted  much  study  and  some  pleasant 
writing.  Incidentally  I was  put  through  my  olfactory  paces 
among  his  herbs  and  acquitted  myself  rather  favourably. 
Our  talk  then  drifted  to  the  use  of  the  sense  of  smell  in 
medicine,  and,  when  I had  quoted  a little  of  my  experience, 
he  urged  me  to  attempt  a review  of  the  subject.  This  I shall 
not  do  here  and  now,  but  my  nose  has  on  many  occasions 
been  so  helpful  to  me  in  conjunction  with  eye  and  car  and 
hand  that  his  urging  did  at  least  prompt  me  to  the  delivery 
of  this  lecture,  in  the  course  of  which  I shnll  have  occasion 
to  consider  some  of  the  distinctive  odours  of  disease.  For 
anything  useful  in  my  remarks  you  must  thank  him;  for 
their  deficiencies — and  descriptions  of  sensory  revelation 
are  not  easy — you  must  blame  me. 

Diagnostic  success  at  the  bedside  may  be  held  to  depend 
firstly  upon  the  historical  analysis,  and  secondly  upon  our 
personal  powers  of  observation,  both  of  which  are  subject 
to  the  continual  leaven  of  experience.  Nothing  is  so  variable 
as  observational  ability.  Some  have  it  well  developed  from 
childhood,  men  of  the  naturalist  type.  Some  never  acquire 
any  facility  for  it,  and  repeatedly  miss  the  obvious.  The 
majority  cultivate  their  aptitudes  by  degrees  and  adopt  a 
middle  level.  Most  of  us  improve  with  time  and  practice, 
but  many  take  but  little  pains  to  refine  and  to  register 
experience,  and,  for  this  reason,  retard  their  progress  in  the 
clinical  arts. 

All  the  five  senses  are  employed  in  observational  medi- 
cine. Taste,  it  is  true,  we  rarely  cnll  to  our  aid  now,  for 
Fehling  and  Benedict  have  relieved  us  of  the  necessity  of 
tasting  the  urine  in  cases  of  diabetes.  The  eyes,  the  hands, 

1 Guy's  Hosp.  Gazette,  1033,  xlrii.  421. 


25 


THE  TRAINING  AND  USE  OF  THE  SENSES 
the  ears,  and  the  nose,  in  that  order,  remain  indispensable, 
and  much  can  be  added  to  their  usefulness  by  training  and  by 
a working  knowledge  of  the  fields  of  perception  open  to  them. 

I shall  throughout  confine  my  attention  to  the  training 
and  use  of  the  unaided  senses.  Just  as  oyer-refinement  or 
an  excess  of  education  may  blunt  the  natural  faculties  of 
the  child,  so,  I believe,  a multiplication  of  the  instrumental 
aids  at  his  disposal  may  serve  to  blunt  the  primary  faculties 
of  the  physician.  I shall  consider  in  turn  sight,  touch,  hear- 
ing, and  smell,  mentioning  some  of  their  opportunities  in 
clinical  work  and  some  of  the  ways  in  which  the  acuity  and 
efficiency  of  each  may  he  improved. 

Sight 

Setting  aside  the  information  gleaned  from  others  we  may 
say  that  diagnosis  begins  the  moment  our  patient  comes 
within  view.  Before  we  have  addressed  a word  to  him  or 
her  we  are,  or  should  be,  taking  mental  notes  of  age, 
physique,  stature,  complexion,  expression,  temperament, 
and,  in  some  cases,  of  peculiarities,  deformities,  or  the  patent 
and  sometimes  specific  surface  evidences  of  disease.  There  is 
a very  genuine  study  in  what  may  be  called  the  physiognomy 
of  disease.  Laycock1  long  ago  gave  particular  attention  to  it. 
Among  the  more  striking  and  specific  physiognomies  we  in- 
clude the  mitral  facies,  with  its  malar  hyperaemia  and  dark 
crimson  lips,  its  varying  tints  of  purple,  and,  when  failure 
is  advanced  and  the  liver  engorged,  its  underlying  icterus. 
The  drawn,  pale,  anxious,  grey-lipped  Hippocratic  facies  of 
peritonitis,  with  * sharp  nose  and  hollow  eyes’,  is  fortunately 
much  rarer  than  it  was,  thanks  to  the  surgeons.  And  so  is 
the  risus  sardonicus  of  tetanus.  The  broad,  thick-lipped, 
impassive  face  of  myxoedema,  with  the  cheeks  tinted  ‘a 
delicate  rose-purple’,  as  Gull  described  it,  a slight  under- 
lying waxiness,  a smoothness  of  the  skin,  and  the  receding 
hair-margin  and  scanty  eyebrows,  is  very  characteristic,  but 
I have  known  it,  when  inspection  was  too  superficial,  mis- 
taken for  that  of  mitral  disease,  nephritis,  or  pernicious 

1 T.  Laycock,  ‘Physiognomical  Diagnosis’,  Med.  Times  and  Gazette,  1802, 
i.  102. 


20  THE  TRAINING  AND  USE  OF  TIIE 

anaemia.  The  anxious  face  of  hyperthyroidism,  with  promi- 
nent eyes  and  bulging  neck,  presents  no  difficulties  in  the 
well-developed  ease,  but  I have  often  had  eases  referred  to 
me  in  which  the  cause  of  a tachycardia  or  a breathlessness, 
a nervousness,  or  a loss  of  weight  had  passed  undetected 
because  slight  and  early  eye-signs  or  the  fine  tremor  of  the 
extended  fingers  had  not  been  observed. 

The  lemon  tint  of  pernicious  anaemia,  not  always  to  be 
readily  distinguished  from  the  more  sallow  tint  of  gastric 
malignancy,  a disease  which  it  may  simulate  in  many  other 
ways,  is  none  the  less  characteristic.  In  gastric  cancer  it  is 
more  likely  that  there  will  be  evidence  of  loss  of  weight, 
with  the  so-called  cachectic  appearance,  and  a slightly  bluish 
nose  is  a frequent  feature.  The  brick-red  facies  of  poly- 
cy  thnemia,  sometimes  simulating  rude  heal  th  at  a firs  t glance, 
but  often  with  a tinge  of  blueness  or  purple  to  modify 
opinion,  is  quickly  confirmed  by  turning  down  the  deep-red 
eyelid  just  as  we  do  in  looking  for  the  conjunctival  pallor 
of  anaemia.  The  watery  eye,  the  blotchy  face,  and  the 
reddish  venous  nose  of  alcoholism,  sometimes  with  tremu- 
lous lips  and  tongue,  may  give  the  clue  to  a correct  inter- 
pretation of  digestive  or  nervous  symptoms.  Acne  rosacea 
may  likewise  prompt  a diagnosis  of  gastritis.  The  slightly 
drooping  lids  and  wrinkled  forehead  of  tabes,  and  the 
Parkinsonian  mask  of  paralysis  ngitans  or  past  encephalitis, 
with  its  flat,  unwinking,  sad,  uncomfortable  lack  of  expres- 
sion (quite  different  from  the  puffy  impassivity  of  myx- 
oedema),  are  strongly  diagnostic.  The  dark  greenish-brown 
of  chronic  obstructive  jaundice,  and  the  dirty  muddy-brown 
pallor  of  uraemia,  whether  due  to  chronic  interstitial  nephri- 
tis in  a young  man  or  to  prostatic  obstruction  in  an  old,  ore 
other  examples  of  diagnostic  colour-change. 

In  acute  disease  there  are  countless  small  accessory  pheno- 
mena for  the  eye  to  observe,  such  as  the  labial  herpes  and 
active  alae  nasi  of  pneumonia;  the  rose-spots  of  typhoid 
fever,  and,  in  grave  cases,  the  involuntary  twitching  of  the 
hand  on  the  coverlet;  the  Stocker’s  sign1  of  meningeal  irrita- 

1 James  Stocker,  an  early  apothecary  to  Goy’a  Hospital  (1831-78),  was 
an  astute  observer  and  drew  attenUon  to  certain  symptoms  of  Irritability 


SENSES  IN  CLINICAL  WORK  27 

tion,  best  shown  in  tuberculous  meningitis ; the  petechiae 
of  blood  diseases  or  infective  endocarditis.  Nor  should  we 
forget  the  clubbed  fingers  of  chronic  lung  disease,  empyema, 
and  infective  endocarditis,  and  the  transverse  grooves  on  the 
nails  which  date  a recent  illness  as  described  by  Wilks. 

But  what  I would  like  to  emphasize  is  that  all  these 
visual  signs  have  their  grades  or  degrees  just  as  the  diseases 
which  they  portray  have  their  stages,  and  it  is  the  early 
changes  we  should  be  more  anxious  to  observe  and  which 
training  and  experience  alone  can  help  us  to  recognize.  It  is 
surely  a much  better  accomplishment  to  ‘spot’  a 60  or  70 
per  cent,  haemoglobin  with  ‘the  naked  eye’  than  a 20  per 
eent.  haemoglobin;  or  an  early  hyperthyroidism  than  a 
‘typical  Graves’.  Book  teaching  is  too  apt  to  impress  us 
with  the  appearances  of  developed  or  advanced  disease. 
And,  apart  from  those  relating  to  structural  or  pigmentary 
modifications,  there  are  the  far  more  difficult,  but  no  less 
valuable,  assessments  relating  to  character,  mood,  and 
temper.  Until,  for  instance,  we  learn  to  read  the  varying 
grades  of  anxiety  or  the  attempts  to  mask  anxiety  and  to 
detect  the  hidden  cancer-phobia  in  the  features  or  behaviour 
of  our  patients,  our  efforts  at  psychological  diagnosis  and 
handling  are  only  partially  rewarded. 

Let  us  now  leave  the  physiognomy  of  disease  and  consider 
other  morbid  aspects,  and  especially  decubitus  and  gaits, 
both  of  which  come  within  the  visual  quarter  of  our  observa- 
tional field.  The  way  the  patient  lies  in  bed  and  the  way  he 
walks  may  tell  us  little  or  much.  You  are  all  familiar  with 
the  orthopnoea  and  dyspnoea  of  cardiac  and  respiratory 
disease.  It  would  take  too  long  to  digress  here  into  the 
many  observable  varieties  of  dyspnoea  which  eye  and  ear 
may  study  conjointly.  The  fixed  rigidity  of  meningitis  is 
easy  enough  to  recognize  in  the  advanced  case.  Its  early 
recognition  in  a case  of  obscure  fever  and  headache  or  in 
subarachnoid  haemorrhage  may  require  the  co-operation  of 

which  distinguished  the  victim  of  meningitis  from  the  more  apathetic  ‘fever’ 
patient.  If,  in  a doubtful  case,  on  attempting  to  raise  the  shirt  to  look  for 
an  eruption  the  patient  assisted  you,  it  was  a case  of  fever ; if  he  resisted  it 
was  one  of  head  disease. 


23  THE  TRAINING  AND  USE  OF  THE 

the  hands,  but  the  decision  to  make  the  further  test  is  often 
prompted  by  the  appearance  of  unwillingness  in  the  patient 
to  move  Ins  head  from  the  pillow.  The  adoption  of  the  knee- 
elbow  position  by  a rheumatic  child  may  be  the  first  sign 
of  pericarditis.  Gull  once  surprised  an  anxious  mother  by 
telling  her  that  her  daughter  with  typhoid  fever  would 
recover  before  he  had  entered  the  sick-room.  He  had  seen 
her  sitting  up  in  bed  as  he  passed  the  door. 

I need  not  describe  to  you  in  detail  here  the  stamping, 
broad-based  action  of  tabes  dorsalis;  the  steppage,  drop- 
foot  gait  of  peripheral  neuritis;  the  dragging  spastic  gait  of 
the  paraplegic  and  the  hemiplegic;  the  festinant  trot  of  the 
paralysis  ngitans;  or  the  stiffening  shuffle  of  old  age.  Their 
enumeration,  however,  brings  me  to  the  question  of  how 
we  may  best  train  our  eyes  to  do  better  as  time  goes  by.  I 
would  first  of  all  tell  you  simply  to  make  a rule  of  having  a 
good  look  at  every  patient  as  he  walks  into  your  presence 
or  sits  or  stands  or  lies  before  you.  To  avoid  embarrassment 
ask  a question  or  two  by  all  means,  but  study  him  well 
meanwhile.  The  art  of  medicine  is  largely  the  art  of  notic- 
ing. You  need  to  cultivate  constantly  both  the  enthusiasm 
and  the  watchful  patience  of  the  field-naturalist  if  you  wish 
to  obtain  the  full  value  and  interest  which  clinical  work  can 
bring.  Secondly,  I would  advise  you — and  it  was  of  this 
that  the  gaits  reminded  me — to  cultivate  the  habit  of*  street- 
diagnosis’.  In  my  ward-clerk  days  I and  some  of  my  con- 
temporaries used  to  compete  in  ‘spotting’  gaits  coming  over 
London  Bridge,  or  facies  sitting  opposite  us  in  the  tube. 
It  is  quite  a good  game,  better  than  crossword  puzzles,  and 
helps  to  pass  the  time  as  well  as  to  train  the  wits.  I often 
used  to  wonder  where  my  social  duty  would  lie  if  I saw  a 
patient  in  the  street  with  a chancre  on  the  lip,  knowing  the 
condition  to  be  dangerous  alike  to  himself  and  others.  At 
last  I was  faced  with  what  looked  like  such  a lesion  in  a 
burly  fellow  travelling  in  a tram.  He  had  a swollen,  oedema- 
tous  lower  lip  with  an  ugly,  hard-looking  scab  on  it  and, 
hoping  to  coax  him  to  Out-Patients,  I made  some  tender 
inquiries,  only  to  find  that  he  had  acquired  it  at  ‘The  Bing’ 
a few  days  previously,  and  that  it  was  merely  the  septic 


SENSES  IN  CLINICAL  WORK  29 

sequel  of  a straight  left.  ‘Spot  diagnoses' — and  please  do 
not  think  that  I am  anxious  for  you  ever  to  depend  on  visual 
diagnosis  alone — are  fallible,  but  our  mistakes  are  salutary 
in  themselves  and  can  be  turned  to  good  account.  In  a walk 
from  the  Borough  to  the  West  End  you  are  hardly  likely  to 
miss  seeing  a few  pathological  gaits  or  an  example  or  two 
of  the  facies  of  anaemia,  alcoholism,  or  malignant  disease. 
You  might  even  keep  a note-book  of  your  ‘bags*  and  con- 
firm your  opinions  by  reference  to  the  text-books  at  bed- 
time. 


Toucn 

The  sensitiveness  of  hands  and  finger-tips  must  be  almost 
as  variable  as  their  character  and  shape.  I believe  we  chiefly 
fail  in  palpation  through  lack  of  the  art  of  ‘ fine  adjustment’, 
to  borrow  a term  from  the  microscope.  It  is  scarcely  ever 
necessary  or  useful  to  examine  forcibly  or  roughly.  Gross 
abnormalities  we  are  only  likely  to  miss  if  we  are  hasty  or 
careless.  But  again  it  is  the  slighter  abnormalities  that  are 
most  valuable  to  us  and  our  patients,  and  these  are  only  to 
be  detected  by  the  cultivation  of  a technique  which  is  at 
once  gentle  and  searching.  The  texture  and  qualities  of  the 
skin  and  the  hair,  whether  we  are  looking  for  myxoedema 
or  testing  the  lost  lustre  in  the  locks  of  an  ailing  child, 
are  assayed  by  the  fingers  as  well  as  the  eyes.  The  slight 
oedema  of  the  skin  over  an  empyema  or  other  deep  sup- 
puration is  more  worthy  of  discovery  than  the  deep  and 
obvious  pitting  of  hydraemic  nephritis,  and  only  the  trained 
and  expectant  thumb  and  forefinger  can  do  it.  The  tiny 
anal  fissure,  so  often  the  cause  of  misleading  and  widely 
distributed  pain  and  quite  commonly  missed,  can  be  appre- 
ciated as  well  by  the  forefinger  as  by  the  speculum;  the 
‘feel’  of  the  lesion  reminds  one  of  the  roughness  of  the 
button-hole  in  the  lapel  of  one's  coat.  In  the  abdomen 
minor  degrees  of  rigidity  or  guarding  can  only  be  appre- 
ciated if  we  cultivate  the  gentle  habit  and  the  flat  hand. 
The  spleen,  so  useful  in  many  diagnoses,  and  so  often  missed 
in  its  lesser  degrees  of  enlargement,  may  escape  our  notice 
through  employment  of  the  finger-tips  instead  of  the  margin 


32 


THE  TRAINING  AND  USE  OF  THE 

You  might  suppose  that  the  ear  would  not  be  of  great 
assistance  in  abdominal  diagnosis,  but  I would  remind  you 
that  it  tells  us  of  hiccups,  a grave  development  in  peritonitis 
and  renal  disease ; that  the  succussion  splash  is  a most  use- 
ful sign  in  pyloric  stenosis;  and  that  there  are  borborygmi 
which  matter  and  borborygmi  which  do  not.  The  com- 
monest are  the  almost  musical  borborygmi  of  the  nervous 
maid  waiting  at  table.  There  is  another  curious  type  of 
rhythmical  bubbling  in  the  stomach,  synchronous  with  the 
respirations,  which  occurs  in  nervous  enteroptotie  women 
who  have  acquired  a faulty  habit  of  abdominal  breathing. 
These  are  gastric  in  origin.  But  there  are  also  intestinal 
borborygmi  of  grave  import  in  chronic  obstruction,  which 
synchronize  with  peristaltic  movements,  subterranean  in 
quality  and  recurring  at  more  or  less  regular  intervals. 
Without  putting  the  ear  to  the  abdominal  wall,  they  may 
be  readily  located  in  the  bowel.  Finally  there  are  sounds 
which  I would  characterize  as  ‘hollow  tinklings which  may 
be  heard  in  cases  of  paralytic  distension  of  the  gut,  or  again 
in  chronic  intestinal  obstruction.  The  sense  of  hearing,  like 
the  sense  of  sight,  can  only  be  trained  and  put  to  better  use 
by  paying  attention,  and  by  deeming  nothing  so  trivial  as 
to  be  allowed  to  escape  your  notice. 

Smell 

Lastly  wc  come  back  to  the  nose.  In  civilized  man  the 
olfactory  sense  has  undoubtedly  lost  a good  deal  of  its 
primitive  acuity.  The  sense  of  smell  is  much  more  easily 
tired  than  the  other  senses.  Unfortunately,  too,  it  is  ex- 
tremely difficult  to  describe  smells.  Colours  and  shades  or 
shapes  may  be  defined  and  given  names;  sounds  may  be 
given  attributes  both  of  quantity  and  quality;  smells  can 
merely  be  likened  to  other  smells ; they  may  6e  given  degrees 
of  goodness  and  badness,  but  our  descriptions  are  sadly 
lacking  in  precision.  I shall  consider  diagnostic  smells  under 
four  headings: 

1.  The  smell  of  the  patient  as  a whole,  as  noted  in  condi- 
tions in  which  we  are  unable  to  assign  the  aroma  to 
any  particular  excretion  or  exhalation. 


33 


SENSES  IN  CLINICAL  WORK 
2.  The  smell  of  the  breath. 

8.  The  smell  of  the  excreta. 

4.  The  smell  of  pathological  discharges. 

In.  the  old  days  when  the  wards  of  the  general  hospitals 
were  largely  filled  with  fever  cases,  it  was  not  uncommon  to 
find  ward  sisters  of  experience  who  could  diagnose  a fever 
from  its  smell.  Typhoid,  diphtheria,  and  measles  have  been 
reputed  to  be  so  recognizable.  Mr.  T.  B.  Layton  has  recently 
told  us  in  the  Gazette  of  a dresser  who  had  a ‘good  nose  * for 
diphtheria.  During  the  First  World  War  I thought  that  I be- 
came familiar  with  the  typhoid  smell,  but  perhaps  through 
lack  of  concentrated  experience  I would  not  guarantee  to 
‘spot5  any  of  the  other  exanthemata  with  my  nose.  I have 
often  thought  that  the  sweat  of  the  phthisical  patient  had 
a particular  odour,  but  I cannot  describe  it.  The  sweat  in 
rheumatic  fever  is  said  to  have  a sour  quality.  Of  other 
specific  smells,  the  skin  disease  Favus  has  the  smell  of  mice. 

The  breath  has  many  important  smells.  The  unpleasant 
breath  of  pyorrhoea  is  by  no  means  the  least  important, 
and  its  presence  may  help  to  clinch  a decision  to  treat 
radically  mouths  in  which  the  outward  appearances  alone 
are  not  at  first  sight  too  bad.  I have  recently  seen  two 
victims  of  general  ill  health,  one  with  a secondary  anaemia, 
in  whom  the  typical  pyorrhoea  odour  at  once  attracted  my 
attention  to  what  was  probably  the  primary  cause.  The 
breath  of  an  alveolar  abscess  and  of  some  antral  suppura- 
tions is  distinctly  more  foul  than  that  of  pyorrhoea. 

Halitosis  from  bowel  and  liver  disturbances  is  entirely 
distinct  in  character  from  the  odours  accompanying  sup- 
puration in  the  mouth.  It  is  stale  and  vaguely  reminiscent 
of  the  smell  of  faeces  or  bowel-wind,  although  quite  dis- 
tinguishable from  them.  In  cases  of  pulmonary  abscess  or 
gangrene  the  breath,  as  well  as  the  sputum,  may  be  as 
putrid  as  anything  encountered  in  medicine. 

Turning  to  more  pleasant  odours,  we  should,  most  of  us, 
be  familiar  with  the  so-called  acetone  odour  of  the  diabetic. 
I find  that  noses  vary  enormously  in  their  ability  to  detect 
this.  My  own  is  rather  acute.  I have  diagnosed  diabetes 
from  the  foot  of  the  bed,  and  I can  detect  the  ketonaemic 


34  TIIE  TRAINING  AND  USE  OF  THE 

breath  in  any  febrile  child.  I have  formed  the  habit  of 
asking  my  ward  clerks  to  smell  the  breaths  of  diabetic 
patients  in  the  wards,  and  when  the  pleasant,  faintly  fruity 
odour  is  evident  to  me  I commonly  find  that  it  is  undetected 
by  something  like  one-third  to  one-half  of  the  firm.  Apart 
from  making  the  diagnosis  of  diabetes  in  the  presence  of 
glycosuria  it  may  also  quickly  settle  the  cause  of  a coma, 
and  so  help  to  save  a life. 

The  uraemic  breath  is  another  important  one,  but  diffi- 
cult to  describe.  It  is  only  moderately  unpleasant.  It  has 
somewhat  fishy  qualities;  it  is  not  exactly  a urinous  smell, 
nnd  yet  it  is  reminiscent  of  urine  just  as  halitosis  is  some- 
how reminiscent  of  bowel  contents.  I have  not  yet  deter- 
mined how  constantly  and  at  what  level  of  the  rising  tide 
of  nitrogen-retention  it  becomes  appreciable  in  the  breath, 
but  it  has  helped  me  to  the  diagnosis  and  prognosis  of  ad- 
vanced renal  disease  nnd  on  several  occasions  to  a recogni- 
tion of  prostatic  uraemia  in  cases  in  which  the  bladder 
symptoms  were  not  pronounced,  the  urine  contained  little 
or  no  albumin,  and  the  general  symptoms  had  previously 
passed  unexplained. 

The  following  case  is  of  particular  interest: 

A man,  aged  50,  was  referred  to  me  by  Dr.  Berry,  of  Watford,  for 
general  malaise,  'vague  discomfort  in  the  liver  region,  loss  of  weight, 
cromps,  and  thirst.  A complete  physical  overhaul  failed  to  reveal 
any  conclusive  signs  of  disease,  but  I made  the  comment  that  his 
breath  had  the  somewhat  fishy  odour  of  uraemia.  His  urine  was 
chemically  normal  and  showed  no  casts,  and  his  blood-pressure  was 
normal.  lie  was  referred  to  Dr.  Hurst’s  Clinic.  Here  the  only  out- 
standing findings  were  a blood-urea  of  103  rogm.  per  100  c.c.  (about 
three  times  normal)  and  a poor  urea  concentration.  He  was  thought 
to  have  a slight  prostatitis,  but  there  was  no  considerable  enlargement 
of  the  gland.  On  a low  protein  diet  he  quickly  lost  all  his  symptoms, 
and  gained  weight,  and  two  and  a half  years  later  was  able  to  perform 
his  full  work  and  to  play  thirty-six  holes  of  golf  each  Saturday  and 
Sunday.  After  two  more  years  of  good  health  this  patient  was  seen  in 
an  acute  illness  due  to  a right-sided  pyonephrosis,  with  pronounced 
uraemia,  but  again  recovered. 

In  cases  of  pyloric  stenosis  and  obstruction  there  are  fre- 
quently eructations  of  sulphuretted  hydrogen.  A description 
of  ‘rotten  eggs’  by  the  patient  or  a relative  has  many  times 


SENSES  IN  CLINICAL  WORK  35 

helped  me  to  suspect  or  confirm,  the  diagnosis.  In.  gastro- 
colic fistula  ‘bowel-wind*  is  eructated. 

It  is  clearly,  on  occasion,  of  the  first  importance  to  detect 
alcohol  and  drugs  such  as  paraldehyde  in  the  breath. 

I have  mentioned  the  exceedingly  putrescent  foulness  of 
the  sputum  in  pulmonary  abscess  and  gangrene.  In  bron- 
chiectasis the  sputum  is  usually  less  foul,  and  it  may  be 
merely  heavy,  mawkish,  and  musty.  In  pulmonary  tuber- 
culosis the  odour  is  slight  and  almost  sweetish. 

The  urine  has  the  same  pleasant  fruitiness  as  the  breath 
in  untreated  diabetes.  In  bacilluria  it  is  characteristically 
unpleasant  and 1 fishy  \ The  damp,  ammoniacal  odour  above 
the  bed  in  urinary  incontinence  may  give  an  early  hint  of 
the  gravity  of  a case  or  in  neurology  of  spinal  cord  involve- 
ment. Faecal  unpleasantnesses  are  very  numerous  and 
variable,  but  in  ulcerative  colitis  they  are  of  a constant 
type  and  particularly  objectionable.  Fatty  stools  from 
pancreatic  or  mesenteric  disease  are  rancid.  The  smell  of 
a ‘faecal  fistula*  discharge  is  distinctive  and  separable  on 
the  one  hand  from  the  ordinary  smell  of  faeces  and  on  the 
other  from  that  of  pus  infected  with  bowel  organisms.  The 
surgeon  draws  useful  conclusions  from  the  relative  sweet- 
ness or  foulness  of  purulent  discharges  both  in  respect  of 
their  nature  and  the  progress  of  the  case.  During  the  First 
World  War  wounds  infected  with  the  organisms  of  gas 
gangrene  were  characteristically  malodorous. 

It  is  a natural  inclination  to  avoid  dalliance  over  patho- 
logical odours,  and  yet  it  is  clearly  our  duty  to  improve  our 
acquaintance  with  them.  I -would  advise  you,  therefore, 
to  train  your  noses  in  respect  of  breaths,  sputa,  and  urines 
in  particular,  and  to  remember  that  they  may  occasionally 
give  you  just  as  valuable  information  as  the  laboratory,  and 
in  much  quicker  time.  The  nose  may  also  be  trained  in  the 
street  and  garden  to  sift  and  analyse  smells  which  are 
ordinarily  passed  by. 

Our  final  opinion,  of  course,  in  any  ease  is  based  upon  a 
compounding  of  sense-data  and  an  analysis  by  the  mind  of 
all  the  information  we  have  collected  by  all  the  means  at 


30  THE  TRAINING  AND  USE  OF  TITE  SENSES 
our  disposal.  The  more  accurately,  however,  we  observe 
with  our  special  senses,  the  more  judicial  will  our  choice  of 
other  methods  be  and  the  more  accurate  the  final  opinion. 
Do  not  think  that  the  few  illustrations  I have  given  you 
are  intended  to  do  more  than  indicate  the  range  of  possibili- 
ties open  to  your  unassisted  eyes,  hands,  ears,  and  nostrils. 
Your  daily  life  in  clinical  medicine  will  furnish  you  •with 
others  in  plenty,  some  which  arc  old  and  familiar  and  others 
which  you  will  reveal  to  yourselves.  I am  conscious  of 
having  omitted  certain  distinctive  observations  now  inacces- 
sible in  the  lumber-room  of  my  memory.  The  fact  that 
they  arc  inaccessible  only  shows  that  I did  not  attend  to 
them  at  the  time  or  register  them  afterwards  as  carefully 
ns  I should.  Nothing  in  medicine  is  so  insignificant  ns  to 
merit  inattention. 


Ill 

THE  CLINICAL  STUDY  OF  PAIN 

WITH  SPECIAL  REFERENCE  TO  THE  PAINS  OF 
VISCERAL  DISEASE1 

Of  all  the  symptoms  for  which  we  are  consulted  pain,  in 
one  form  or  another,  is  the  most  frequent  and  frequently 
the  most  urgent.  Properly  assessed  it  stands  pre-eminent 
among  the  sensory  phenomena  of  disease  as  a guide  to 
diagnosis.  And  yet  it  must  be  confessed  that  our  under- 
standing of  its  nature  and  mechanisms,  and  consequently  of 
its  full  significance  in  practice,  remains  peculiarly  limited. 
We  are  naturally  dissatisfied  with  invisible  and  imponder- 
able evidence,  and  it  is  therefore  no  matter  for  surprise  that 
recent  years  have  witnessed  the  introduction  into  medicine 
of  a host  of  objective  methods  of  studying  disease,  and  that 
the  study  of  subjective  symptoms  has  suffered  contem- 
porary neglect.  The  opaque  meal  and  enema ; pyelography ; 
cholecystography;  the  electro-cardiograph;  methods  of 
blood  analysis ; the  various  chemical  tests  for  gastric,  hepa- 
tic, pancreatic,  and  renal  efficiency;  bronchoscopy;  lumbar 
puncture  and  its  developments ; and  the  exploratory  opera- 
tion— all  these,  following  in  the  trail  of  the  stethoscope  and 
the  ophthalmoscope  and  older  routine  methods  of  physical 
examination,  bear  witness  to  our  zest  for  objective  informa- 
tion. It  is,  however,  chastening  to  remind  ourselves  that, 
notwithstanding  all  the  help  derived  from  a judicial  em- 
ployment of  them,  these  methods  too  have  their  limitations, 
and  none  of  them  is  infallible.  They  are  often  useful  in 
proving  or  disproving  the  existence  of  established  organic 
disease;  in  increasing  the  accuracy  of  a clinical  opinion; 
and  in  serving  to  differentiate  one  form  of  organic  disease 
from  another.  They  have  greatly  helped  in  decisions  for 
or  against  operative  intervention.  They  have  undoubtedly 
exerted  an  instructive  and  a corrective  influence.  In  some 
degree— although,  to  my  mind,  by  no  means  so  much  as 

1 Brit  Med.  Joum.,  1028.  L 537. 


28  TIIE  CLINICAL  STUDY  OF  TAIN 

they  might  have  done — they  have  even  enhanced  our  appre- 
ciation of  subjective  symptoms.  But  their  contributions  to 
the  early  diagnosis  of  organic  disease  and  to  the  study  of 
functional  disorders  are  necessarily  restricted,  and  it  is  clear 
that  without  the  initial  indication  of  certain  symptoms 
they  could  never  be  rationally  employed.  Moreover,  their 
aid  can  rarely  be  invoked  in  urgent  problems  or  in  the 
homes  of  the  people.  There  is  a very  real  danger  that  by 
over-reliance  on  them,  by  too  gTeat  an  anxiety  to  give  our 
patients  the  benefit  of  modem  investigations,  and  by  a 
waning  confidence  in  our  own  clinical  ability,  we  may  come 
to  lose  the  astuteness  and  wisdom  of  our  forebears. 

In  medical  education  the  introduction  of  these  methods 
has  not  been  an  unqualified  blessing,  and  the  training  of 
ear  and  eye  and  hand  and  the  development  of  the  power  of 
inductive  reasoning  have  suffered  much.  Every  year  I see 
a number  of  mistakes  made  through  inappropriate,  un- 
necessary, or  excessive  investigation.  Not  infrequently  I 
have  myself  fallen  into  error  for  similar  reasons;  and  not 
infrequently  I have  extricated  myself  from  error  by  a return 
to  first  principles,  by  taking  the  history  of  the  case  again, 
or  by  making  a more  careful  analysis  of  the  patient’s  sensa- 
tions— Nature’s  earliest  signals  of  morbidity.  It  will  be 
readily  agreed  that  many  of  the  best  diagnoses  and  judge- 
ments are  achieved  with  the  unaided  senses  backed  by 
experience.  It  will  also  be  agreed  that  no  course  of  action 
can  train  these  senses  unless  it  includes  experience  patiently 
garnered  at  the  bedside  and  in  the  consulting-room. 

If  I were  asked  how  the  next  considerable  advance  is  to 
be  sought  and  won  in  the  field  of  clinical  medicine  I should 
say  (with  grateful  acknowledgements  to  the  influence  of  Sir 
James  Mackenzie)  by  the  intimate  study  of  the  physiology 
of  symptoms,  and  (once  more  acknowledging  our  debt  to 
other  great  pioneers  in  this  field — notably  John  Hilton  and 
Sir  Henry  Head)  I would  submit  that  our  first  concern 
should  be  a more  extended  and  intimate  study  of  pain. 

This  brings  me  to  a consideration  of  method.  Now,  re- 
search into  subjective  phenomena  does  not  commend  itself 
to  the  laboratory  worker,  and  cannot  easily  be  pursued  in 


THE  CLINICAL  STUDY  OF  PAIN  39 

the  experimental  animal.  It  is  presumably  for  this  reason 
that  even  the  more  recent  text-books  of  physiology  are 
extraordinarily  reticent  on  the  subject  of  all  excepting  the 
superficial  pains,  and  that  the  scanty  references  which  they 
make  to  visceral  pain  are  often  misleading.  Thus  they 
nearly  all  declare  that  visceral  pain  is  very  inaccurately 
located,  and  devote  more  discussion  to  the  occasional  sym- 
pathetic or  somatic  than  to  the  far  more  frequent  visceral 
sensations.  Experiments  on  the  healthy  human  subject, 
such  as  those  conducted  by  Hurst  and  his  collaborators  in 
the  course  of  their  work  on  the  sensibility  of  the  alimentary 
canal,  are  of  necessity  limited,  and  no  amount  of  ingenuity 
can  quite  reproduce  the  experiments  in  disturbed  sensation 
with  which  Nature  herself  provides  us  in  our  own  bodies  or 
those  of  our  patients.  The  study  of  pain  must  therefore 
continue  to  devolve  mainly  upon  the  clinicians. 

I wish  that  time  would  permit  me  to  refer  to  the  method 
and  the  classical  contributions  of  the  pioneers  whose  names 
I have  mentioned,  and  to  the  valuable  communications  of 
others,  including  Ross,  Morley,  and  Cope  in  this  country, 
and  of  Lennander,  Rudolf  Schmidt,  and  others  abroad.  For 
my  present  purpose  let  it  suffice  to  recall  that,  whatever  the 
individual  trend  of  these  investigators  may  have  been — 
whether  anatomical,  physiological,  surgical,  or  neurological 
— the  basis  of  all  their  researches  was  clinical  observation. 

Partly  because  the  immensity  of  the  subject  compels 
selective  treatment,  partly  because  visceral  pains  have  espe- 
cially  interested  me  in  my  work  as  a general  physician,  and 
partly  because  they  seem  to  me  to  have  suffered  neglect  in 
comparison,  for  instance,  with  the  pains  of  nervous  disease, 
I have  chosen  to  confine  my  attention  in  this  paper  to  the 
subject  of  pain  expressing  visceral  disease.  My  remarks  will 
fall  into  three  sections.  In  the  first  I shall  endeavour  to 
summarize  the  present  state  of  our  knowledge  of  the  physio- 
logy of  pains  affecting  the  hollow  organs.  In  the  second  I 
shall  outline  a simple  system  for  the  clinical  analysis  of 
such  pains — a system  which  really  embodies  nothing  new, 
and  which  is  in  large  measure  applicable  to  the  study  of 
other  pains.  In  the  third  I shall  consider,  with  examples. 


40  THE  CLINICAL  STUDY  OF  PAIN 

the  practical  applications  of  pain  analyses,  for,  after  all, 
the  chief  interest  to  the  practising  part  of  our  profession  of 
all  such  studies  is  their  bearing  upon  the  advancement  of 
diagnosis,  prognosis,  and  treatment. 

Visceral  Pain 

The  insensitiveness  to  ordinary  tactile,  thermal,  and 
chemical  stimuli  of  the  serous  and  mucous  coats  of  the 
hollow  viscera  has  been  established  in  various  ways.  Partly 
on  this  account  Sir  James  Mackenzie  became  protagonist  for 
the  view  that  there  is  no  true  visceral  pain,  but  only  pain 
projected  to  the  somatic  tissues  supplied  by  the  same  seg- 
ment of  the  cord  as  that  which  supplies  the  injured  viscus. 
This  view  still  finds  a few  supporters,  but  common  ex- 
perience and  experiment  have  rendered  it  untenable  for 
the  majority  of  students.  There  is  reason  to  believe  that 
Mackenzie  latterly  modified  his  earlier  view  to  that  more 
generally  upheld,  for  in  1922,  in  response  to  certain  observa- 
tions of  my  own,  he  wrote  to  me  as  follows:  ‘It  is  to  answer 
this  question  that  I have  spent  a long  inquiry  and  have 
come  to  the  conclusion  that  the  only  known  stimulus  that 
produces  pain  in  the  tissues  which  arc  supplied  only  by 
the  autonomic  nerves  is  the  contraction  of  muscle.  ’ I would 
prefer,  for  reasons  which  will  become  apparent,  that  we 
should  state  the  matter  a little  differently  by  saying  that 
‘visceral  pain  is  commonly  due  to  an  abnormal  increase  in 
tension  in  the  muscular  element  of  the  wall  of  the  viscus’, 
for  a positive  contraction  is  not  the  only  cause  of  increased 
tension  or  of  pain.1 

This  conception  of  the  cause  of  visceral  pain  can  be 
equally  well  adduced  in  explanation  of  pains  as  diverse  in 
character  and  circumstance  as  those  of  labour,  of  gastric 
ulcer,  and  of  renal  colic.  But  there  are  other  observations 
accessory  to  the  main  conclusion  which  may  be  made  in 
regard  to  the  pains  of  visceral  disease.  These  I shall 

1 In  cardiac  pain  ischaemia  (or  the  associated  chemical  accompaniments 
of  ischaemia)  would  appear  to  be  the  main  factor,  and  it  is  possible  that 
the  ischaemia  with  demonstrable  pallor  which  accompanies  muscle  spasm 
may  be  a more  important  immediate  cause  of  pain  than  the  shortening 
of  the  muscle-fibre. 


THE  CLINICAL  STUDY  OF  PAIN 


41 


summarize  as  concisely  as  possible,  referring  to  them  as 
‘laws’  of  visceral  pain  for  brevity  and  convenience,  and 
implying  thereby  ‘present  beliefs’  rather  than  ‘unalterable 
truths’. 


‘ Laws'  of  Visceral  Pain 

(1)  Visceral  pain  has  its  origin  in  and  is  due  to  an  abnormal  increase 
in  tension  of  the  muscular  element  of  the  wall  of  the  viscus,  this  in* 
crease  in  tension  resulting  either  (a)  from  contraction  of  the  muscle, 
or  {&)  from  its  failure  to  relax  in  the  face  of  increasing  intravisceral 
pressure.  (Examples : (a)  tonic  spasm  of  the  colon,  ({>)  bladder  pain 
in  the  early  stages  of  retention  before  the  muscle-fibres  have  become 
overstretched.) 

(2)  Relieving  factors  in  visceral  pain,  other  than  those  which 
merely  deaden  consciousness,  are  invariably  factors  which  reduce 
intravisceral  pressure  or  encourage  muscular  relaxation.  (Examples: 
the  relief  of  pain  from  the  sudden  perforation  of  a diseased  appendix; 
the  passage  of  a calculus ; the  taking  of  food  in  duodenal  ulcer.) 

(3)  As  would  he  anticipated  if  the  truth  of  (I)  and  (2)  is  conceded, 
the  severity  of  mechanically  induced  pain  is  in  inverse  proportion  to 
the  normal  distensibility  of  the  viscus.  (Thus  the  most  severe  pains 
are  found  in  disease  involving  tubes  of  small  calibre  and  small  dis- 
tensibility, such  as  the  uTeter,  the  bile  ducts,  and  the  arteries;  the 
more  bearable  pains  in  disease  involving  organs  of  wide  calibre  and 
a wide  range  of  physiological  distensibility  and  postural  adaptability, 
such  as  the  stomach  and  urinary  bladder.) 

(4)  Visceral  pain  when  occurring  alone  or  dissociable  from  atten- 
dant pains  in  the  somatic  tissues  or  other  viscera  can  be  accurately 
located  by  the  patient,  the  localization  corresponding,  not  with  any 
segmental  nerve  distribution,  but  with  the  surface  marking  of  the 
viscus.  (Examples : the  loin  gesture  of  renal  pain ; the  sternal  gesture 
of  cardiac  pain ; the  accurate  indication  of  the  point  of  obstruction  in 
oesophageal  and  some  colonic  strictures.) 

(5)  Visceral  pain,  having  its  origin  in  muscle,  is  related  to  the 
functional  activity  of  the  affected  viscus.  (Thus  it  is  increased  or 
relieved  by  food  or  fasting  in  gastric  and  duodenal  ulcer,  by  effort  or 
rest  in  cardiovascular  disease,  just  as  pain  in  skeletal  muscle  is 
aggravated  by  use  and  relieved  by  rest.) 

(6)  Referred  somatic  pain  or  soreness  in  visceral  disease  may  ac- 
company (a)  severe  visceral  crises  of  mechanical  origin,  (6)  inflamma- 
tory or  ulcerative  disease  of  the  visceral  wall,  and  more  particularly 
if  this  involves  the  muscular  coat.  (Examples : (a)  arm  pain  in  angina 
and  testicular  pain  in  ureteric  colic ; (6)  cutaneous  soreness  in  appendi- 
citis and  chronic  gastric  ulcer.) 

(7)  Sustained  somatic  pain  or  soreness  in  visceral  disease  persisting 
apart  from  recent  crises  of  viscera!  pain  implies  inflammatory  disease 


42  THE  CLINICAL  STUDY  OF  PAIN 

of  the  viscus  in  question.  (Example:  scapular  angle  pain  and  inter- 
scapular pain  and  soreness  in  chronic  cholecystitis.) 

(8)  Conversely,  absence  of  somatic  pains  and  soreness  is  the  rule 
in  cases  of  visceral  pain  dependent  on  functional  derangements  or 
due  to  obstructive  lesions  in  the  more  distensible  viscera.  (Examples; 
chronic  colon  spasm ; pyloric  or  colonic  growths.) 

It  need  hardly  be  remarked  that  in  actual  practice  we 
often  encounter  confusing  effects  which  result  from  the  ex- 
tension of  disease  or  multiple  lesions  or  from  the  ‘spread1 
of  pain  due  to  temperamental  factors  or  long-continued 
psychological  or  physical  ill  health.  Such  a qualification 
need  not,  however,  damage  these  main  conclusions.  It 
would  be  impossible  to  detail  here  the  accumulated  evidence 
on  the  basis  of  which  it  1ms  seemed  justifiable  to  formulate 
the  foregoing  ‘laws’. 

The  referred  sensory  phenomena,  requiring  for  their 
production  special  circumstances,  such  ns  intensity  or  pro- 
longation through  on  inflammatory  process  of  the  appro- 
priate stimulus,  arc  infrequent  in  comparison  with  the  local 
phenomena,  and  so  are  of  less  constant  diagnostic  value. 
It  would  therefore  seem  fitting  to  devote  our  attention  more 
particularly  to  the  primary  visceral  pains.  It  is  chiefly  with 
these  that  I shall  concern  myself  in  outlining  the  scheme  for 
the  analysis  of  a pain  which  follows. 

TnE  Analysis  of  a Pain 

When  a patient  comes  to  us  with  a complaint  of  pain  it 
is  customary  and  natural  to  ask  him  where  the  pain  is  felt 
and  what  its  character  may  be.  Each  of  us,  no  doubt,  has 
his  individual  method  of  approach.  Often  a few  direct 
questions  and  a little  patience  will  elicit  replies  so  informa- 
tive as  to  put  us  immediately  on  the  track  of  an  accurate 
opinion,  but  there  remain  a host  of  ‘difficult  pains’  in  which 
our  simple  routine  brings  no  reward,  and  we  are  left  ‘ wonder- 
ing*, or  are  compelled  to  proceed  to  the  physical  examina- 
tion, which  may,  in  its  turn,  prove  exnsperatingly  negative. 
Even  the  ‘further  investigations’,  when  we  can  indulge  in 
such  luxuries  or  send  the  case  to  hospital,  do  not  necessarily 
supply  the  answer  to  our  problem.  It  is  just  in  these  cases 


THE  CLINICAL  STUDY  OF  PAIN  43 

that  we  feel  the  need  for  some  fuller  method  of  inquiry.  A 
little  reflection  will  show  that  there  are  no  less  than  ten 
reasonable  Questions  which  may  be  propounded  in  any  given 
case  of  visceral  pain,  and,  indeed,  of  most  other  kinds  of  pain. 
Each  of  these  questions  has  some  direct  bearing  on  the 
qualities  or  circumstances  of  the  symptom,  and  so  renders 
our  investigation  less  haphazard.  It  is  true  that  the  answers 
to  these  questions  must  be  accorded  very  variable  marks 
for  merit.  We  cannot  expect  to  obtain  consecutive  or 
intelligent  co-operation  from  all  our  patients,  but  this  is 
no  reason  for  abandoning  the  attempt.  For  our  failures  to 
‘establish  contact’  or  to  assess  the  reliability  of  replies  we 
must  hold  ourselves  at  least  in  part  to  blame,  and,  profiting 
by  them,  must  aim  at  an  improved  technique. 

Of  these  ten  questions  two  have  a bearing  on  quality  and 
quantity,  and  may  be  answered  under  the  headings  of 
(1)  character  and  (2)  severity.  Three  have  a bearing  on  spa- 
tial relationships,  and  are  answerable  under  the  headings 
of  (8)  situation  (including  depth  from  the  surface),  (4) 
localization  (or  extent  of  diffusion),  and  (5)  paths  of  refer- 
ence. Three  have  a bearing  on  temporal  relationships,  and 
are  answerable  under  the  headings  of  (6)  duration,  (7)  fre- 
quency, and  (8)  special  times  of  occurrence.  Two  have  a 
bearing  on  determining  causes,  and  are  answerable  under 
the  headings  of  (9)  aggravating  and  (10)  relieving  factors. 
Over  and  above  these  questions  directly  relating  to  the  pain 
our  interrogatory  must  also  include  associated  symptoms.  All 
of  these  questions  are  concerned  with  the  spontaneous  pain 
experienced  by  the  patient.  At  a later  stage  we  proceed  to 
examine  for  elicited  visceral  pain  (or  ‘tenderness’)  and 
elicited  somatic  pain  (or  ‘soreness’). 

Practical  Applications 

Now  let  us  consider  the  practical  utility  of  an  analysis  of 
this  kind.  What  can  we  learn  of  the  character  of  a pain  ? 
It  is  common  knowledge  that  certain  descriptive  adjectives 
crop  up  again  and  again  in  the  language  of  our  patients, 
and  these  must  be  accorded  their  full  due.  Thus  the  pain 
of  ulcer  is  usually 1 gnawing  ’ or  of  a dull  * toothache  * quality ; 


41  THE  CLINICAL  STUDY  OF  FAIN 

it  is  sustained  while  it  lasts — that  is  to  say,  it  is  not  markedly 
fluctuating  and  never  intermittent.  In  an  acute  irritative 
gastritis  the  pain  may  be  peristaltic  and  intermittent.  The 
secondary  gastric  pain  of  gall-stone  dyspepsia  is  commonly 
of  a ‘bursting*  character.  The  pain  of  angina  pectoris, 
sometimes  so  agonizing  as  to  defy  description,  is  often  re* 
ferred  to  as  ‘crushing’,  or  ‘viee-like*.  The  pains  of  biliary 
and  renal  colic,  devastating  in  their  ultimate  throes,  are 
nearly  always  continuous  and  crescendo,  and  in  no  true 
sense  ‘colicky’;  they  start  with  a dull  ache  which  becomes 
progressively  more  intolerable.  The  pain  of  enteritis  or 
small  intestinal  obstruction  is  truly  ‘colicky’ — that  is  to 
say,  rhythmically  intermittent,  sharp,  and  griping  while  in 
action,  but  quickly  giving  place  to  case  between  the  spasms. 
‘Burning ' pains  are  rarely  indicative  of  gross  organic  disease. 
The  most  familiar  example  is  the  homely  heartburn,  with 
its  unpleasant,  but  never  agonizing,  sense  of  a retrosternal 
and  almost ‘chemical’ heat,  although  such  evidence  as  we 
have  suggests  that  it  is,  in  common  with  strangury  and 
tenesmus,  an  accompaniment  of  spasm.  Diffuse  abdominal 
burning  sensations  arc  chiefly  encountered  in  depressed  or 
emotional  patients. 

The  severity  of  a pain  is  notoriously  hard  to  measure. 
It  is  always  well  to  discover  from  our  patient  at  an  early 
stage  whether  ‘pain’  or  ‘discomfort’  is  the  more  appro- 
priate description.  True  pain  is  more  likely  to  mean  organic 
disease.  Pains  which  arc  comparable  with  or  worse  than 
those  of  labour  or  which  have  required  a hypodermic  in- 
jection we  accept  as  genuinely  severe.  The  effect  of  the  pain 
on  the  performance  of  daily  duties  or  mental  work  or 
equanimity  or  sleep  allows  some  estimate  of  its  gravity. 
Recourse  to  hot  bottles,  or  bed,  or  analgesic  drugs  may 
help  in  our  assessment,  but  in  this  part  of  our  inquiry’  more 
than  any  other  our  own  observational  pow  ers  in  regard  to 
temperament  or  other  factors  likely  to  raise  or  lower  the 
‘threshold’  of  the  individual  to  pain  must  be  called  into  play. 

The  situation  and  localization  of  a pain  are  best  deter- 
mined by  observing  the  patient’s  gesture,  and,  best  of  all, 
when  the  opportunity  cab  be  found,  or  made,  to  see  him  in 


THE  CLINICAL  STUDY  OF  PAIN  45 

its  grip.  The  more  defined  and  accurately  localized  the 
lesion  responsible  for  a visceral  pain  the  more  accurate  and 
defined,  as  a rule,  is  the  gesture  of  the  patient.  There  are 
many  significant  gestures.  A famous  proprietary  pill  has 
caught  in  its  advertisements  the  typical  gesture  employed 
by  the  victims  of  a kidney  stone.  The  pain  of  ulcer  is  com- 
monly indicated  with  the  tips  of  the  fingers  applied  to  mid- 
epigastrium ; the  pain  of  a functional  dyspepsia  with  the  flat 
of  a roving  hand.  The  point  of  arrest  of  a ureteric  calculus 
may  sometimes  be  shown  with  a single  finger.  In  cases  of 
chronic  colon  spasm  I have  seen  the  course  of  the  colon 
accurately  traced  by  patients  wholly  ignorant  of  anatomy. 
Among  the  best  recognized  paths  of  reference  are  those 
involving  the  left  arm  in  angina  pectoris,  sometimes  ex- 
tending to  the  right  arm,  and  in  either  case  usually  confined 
to  the  inner  aspect  and  reaching  the  elbow,  the  wrist,  or 
even  the  ring  and  little  fingers,  and  sometimes  also  rising 
to  the  neck  or  jaw;  the  scapular  or  interscapular  pain  (not 
shoulder  pain)  of  gall-bladder  disease;  and  the  testicular 
pain  of  ureteric  colic.  Superficial  and  more  often  deep  skin 
soreness  may  be  of  very  real  assistance  in  the  diagnosis  of 
gastric  and  duodenal  ulcer,  of  some  forms  of  appendicitis, 
of  cholecystitis,  and  diverticulitis.  Referred  pain  down  the 
front  of  the  thighs  may  accompany  salpingitis  and  tubal 
pregnancy.  The  details  of  the  search  for  zones  of  soreness 
have  received  full  discussion  in  the  literature  and  need  not 
be  considered  here.  Care  is  sometimes  necessary  to  avoid 
confusion  of  a fibrositic  tenderness  with  a true  sympathetic 
hyperalgesia. 

The  duration  of  a pain  has  a very  special  significance,  and 
may  frequently  throw  light  on  the  particular  perturbation 
of  function  which  the  pain  itself  less  surely  expresses.  Thus 
the  intermittent  pains  of  intestinal  colic,  so  clearly  due  to 
peristaltic  over-activity,  last  a few  seconds  only.  The  pains 
of  an  anginal  seizure  (excluding  the  sustained  agony  of 
coronary  occlusion)  rarely  last  more  than  a few  minutes, 
and  are  relieved  by  the  immobility  which  they  compel. 
The  pains  of  gastric  and  duodenal  ulcer  last  an  hour  or 
more,  until  the  stomach  is  empty  or  replenished.  Biliary 


4G  TIIE  CLINICAL  STUDY  OF  PAIN 

and  renal  crises  may  continue  for  an  hour  or  hours,  and 
often  enough  until  the  blessed  relief  of  morphine  has  been 
won.  In  each  instance  we  can  nicely  correlate  the  time 
character  with  the  physiological  event. 

The  frequency  and  special  limes  of  occurrence  of  a pain 
are  also  instructive.  Epigastric  pain  which  recurs  daily  and 
with  some  constant  time  relationship  to  meals  is  almost 
certainly  of  gastric  origin.  Epigastric  pain  arriving  at  rare 
intervals,  ‘out  of  the  blue’,  and  independently  of  eating  or 
other  physiological  exercise,  should  raise  a suspicion  of  gall- 
stones or  tabetic  crises.  Epigastric  pain,  absent  at  times  of 
rest  but  immediately  induced  by  certain  efforts,  is  almost 
undoubtedly  due  to  cardiovascular  disease.  Of  special  limes 
of  occurrence  it  is  also  noteworthy  that  angina,  in  concert 
with  other  ‘spasmodic  complaints’,  as  observed  by  Heber- 
den,  has  a predilection  for  the  early  hours  of  the  morning 
after  the  first  sleep.  The  hunger  pains  of  duodenal  ulcer 
often  wake  their  victims  between  the  hours  of  midnight 
and  2 a.m.,  and  gall-stone  pains  at  a somewhat  later  hour. 

Among  aggravating  factors  (taking  again  the  better-known 
types  of  pain)  exertion,  cold,  annoyance,  and  particularly 
exertion  after  food,  may  all  be  provocative  of  anginal 
seizures.  Jolting  is  apt  to  evoke  pain  in  cases  of  biliary, 
renal,  and  vesical  calculus,  and  in  sufferers  from  chronic 
colon  spasm,  a disorder  which  is  highly  responsive  also  to  the 
influence  of  cold,  fatigue,  worry,  tobacco,  and  purgatives. 
Gentle  thumping  of  the  loin  irill  more  readily  evoke  the 
pain  of  calculous  renal  disease  than  simple  deep  palpation. 
Of  relieving  factors  rest  of  body  and  mind  and  warmth  are 
common  to  the  majority  of  painful  visceral  disorders.  Amyl 
nitrite  has  an  almost  specific  effect  in  anginal  pain,  but  not 
so  in  the  status  anginosus  of  coronary  occlusion.  Alkalis 
and  belladonna  (both  probably  by  facilitating  pyloric  relaxa- 
tion) have  a well-known  efficacy  in  gastric  pain.  Abdominal 
pressure,  ill  tolerated  in  inflammatory  abdominal  disease, 
may  alleviate  the  pain  of  intestinal  colic. 

Now  I would  not  for  a moment  have  it  supposed  that  an 
interrogatory  such  as  I have  outlined  can  be  employed  by 
every  busy  physician  In  every  case  of  visceral  pain  with 


47 


THE  CLINICAL  STUDY  OF  PAIN 
which  he  is  confronted ; but  I would  suggest  that  some  such 
method  is  not  only  appropriate  but  essential  if  we  are  to 
prosecute  a careful  inquiry  into  any  single  type  of  pain ; 
and  further,  that  it  may  be  of  decided  value  in  practice  in 
elucidating  what  I have  described  as  ‘difficult  pains’,  and 
more  particularly  in  those  unhappily  plentiful  cases  of 
chronic  abdominal  disease  in  which  physical  signs  are 
scanty  or  altogether  lacking.  I can  think  of  nothing  better 
calculated  to  stay  the  epidemic  of  injudicious  abdominal 
operations  than  an  extension  of  interest  in  pain  as  a 
diagnostic  symptom. 

If  I were  asked  to  enunciate  a few  important  principles 
for  the  everyday  clinical  study  of  pain  my  choice  would 
fall  upon  the  following: 

First,  in  obscure  cases  and  important  decisions  to  try, 
whenever  possible,  to  see  the  patient  when  his  pain  is 
present,  for  then,  and  then  only,  will  his  own  observations 
be  accurate  and  reliable,  and  not  dependent  upon  memory, 
and  physical  signs,  absent  at  other  times,  may  be  in  evi- 
dence. We  all  know  how  few  and  far  between  (especially 
in  consulting  and  hospital  practice)  are  these  opportunities 
of  seeing  our  patients  in  pain.  This  circumstance  alone  is 
evidence  of  the  rarity  of  continuous  pain  (excepting  in  ad- 
vanced inflammatory  and  malignant  disease),  and  supports 
the  contention  that  visceral  pains  come  and  go  in  a physio- 
logical sequence  and  in  obedience  to  physical  laws. 

Secondly,  to  pay  particular  attention  to  the  patient’s 
gesture,  and,  if  he  makes  none  spontaneously,  to  ask  for  a 
manual  demonstration  with  the  clothes  removed.  ‘A  pain 
in  the  stomach’  may  mean  a pain  anywhere  between  the 
manubrium  stemi  and  the  symphysis  pubis,  and  our  en- 
deavour must  ever  be  in  the  direction  of  greater  accuracy. 
I have  several  times  seen  the  mistake  made  of  supposing  a 
pain  to  be  gastric  because  it  was  related  to  food.  Colonic 
pains  may  also  be  influenced  for  better  or  worse  by  food, 
but  they  are  situated  in  the  lower  abdomen,  whereas  gastric 
pains  are  always  epigastric. 

Thirdly,  to  remember  the  close  association  which  exists 
between  visceral  pain  and  the  functional  activity  of  the 


48  THE  CLINICAL  STUDY  OP  PAIN 

viscus  in  question.  I once  had  a case  referred  to  me  by  a 
cardiologist  on  n suspicion  ol  stomach  trouble  with  a request 
for  a gastric  analysis.  The  patient  was  on  elderly  man  com- 
plaining of  high  epigastric  pain  after  food.  Before  examin- 
ing him  I ascertained  that  the  same  pain  was  also  evoked 
by  walking,  and  that  the  case  was  undoubtedly  one  of 
angina  pectoris. 

It  remains  for  me  to  cite  from  my  personal  store  a few 
case  histories  which  serve  to  show  the  value  of  a full  analy- 
sis of  pain,  and  how  such  an  analysis  may  lead  to  a more 
correct  opinion  or  may  modify  judgement  or  treatment  in 
important  ways.  I have  been  careful  to  include  mistakes 
of  my  own  as  well  as  those  of  others.  IIow  often  these  mis- 
takes give  us  insight  into  matters  previously  debatable  or 
obscure  I 

Case  1.  A ease  in  schich  examination  of  the  patient  during  an  attack 
of  pain  altered  the  diagnosis  from  duodenal  ulcer  to  gall-stones. 

A surgeon  consulted  me  in  1025  for  symptoms  which  had  troubled 
him  at  intervals  since  1017.  His  main  complaint  was  of  epigastric 
pain,  relieved  by  food  and  alkalis  and  occasionally  waking  him  at 
2 o.m.  He  always  carried  alkaline  lozenges  in  ills  pocket.  J found 
slight  hut  definite  tenderness  and  muscular  guarding  below  the  right 
ribs.  A radiologist  who  examined  him  on  two  occasions  reported  some 
irregularity  of  the  duodenal  cap,  but  would  not  commit  himself  to  a 
diagnosis  of  ulcer.  A fractional  test-meal  showed  a slight  degree  of 
liyperclilorhydria.  I diagnosed  duodenal  ulcer.  On  the  strength  of 
a long  history  and  frequent  recent  recurrences,  I was  inclined  to 
advise  operation,  but  it  was  finally  agreed  that  he  should  lie  up  and  . 
undergo  a strict  medical  treatment  as  for  ulcer.  A few  days  after 
storting  the  treatment  he  developed  a severe  epigastric  ache  which 
persisted  for  more  than  two  hours  in  spite  of  alkalis  and  vomiting. 
Morphine  was  given  for  the  relief  of  pain,  which  returned  at  5 ajn. 
the  next  morning.  At  8 a.m.  I saw  him  again  and  was  able  to  feel 
an  enlarged  gall-bladder.  There  was  no  pyrexia  or  icterus.  A week 
later  Mr.  It.  P.  Rowlands  removed  a ttiickened  gall-bladder  with 
stones.  The  duodenum  was  healthy. 

In  referring  to  my  original  notes  of  his  case  I then  found  one 
significant  entry  which  should  have  impressed  me  more.  Jn  the  earlier 
days  of  his  complaint  the  pain,  although  related  to  food,  seas  interscapular 
and  not  epigastric.  There  was  also  a history  of  typhoid  fever  14 years 
before  the  first  development  of  symptoms. 

Case  2.  A case  in  schich  the  severity  of  the  pain  led  to  a diagnosis  of 
gall-stones  and  a fruitless  operation;  in  schich  a radiologist  later  diag - 


49 


THE  CLINICAL  STUDY  OF  PAIN 
nosed  lesser  curvature  ulcer;  but  in  which  the  clinical  analysis  led  to  a 
correct  diagnosis  of  * chronic  posterior  duodenal  ulcer  adherent  to  the 
pancreas  \ 

A fine  old  soldier  of  73  had  suffered  from  periodic  bouts  of  epi- 
gastric pain  for  more  than  6 years.  Latterly  these  had  become  more 
severe  and  incapacitating.  In  the  attacks  he  ‘shook  all  over’  and 
the  pain  compelled  him  to  cry  out.  He  saw  a surgeon  who  diagnosed 
gall-stones,  and  notwithstanding  a negative  cholecystogram  and  a 
failure  to  discover  stones  at  the  operation  he  elected  to  drain  the 
gall-bladder.  After  the  operation  the  pain  returned  and  was  as  bad 
as  ever.  I then  saw  the  patient  and  made  the  following  entries  in 
my  notes:  At  an  earlier  stage  the  pains  came  at  a long  interval  after 
food  and  were  relieved  by  food . They  were  more  troublesome  at  night. 
The  pain  in  the  bad  attacks  now  goes  through  to  the  back  at  the  same 
level  on  the  right  side,  i.e.  at  the  level  of  the  11th  or  12th  rib  and  not  at 
the  scapular  angle.  There  teas  slight  guarding  with  deep  tenderness  at 
the  duodenal,  not  at  the  gall-bladder  point.  Finally,  during  convalescence 
from  the  operation,  he  had  twice  had  melaena.  Clearly  this  last  symp- 
tom made  it  very  much  easier  for  me,  but  I also  had  the  good  fortune 
to  be  familiar  with  the  excessively  severe  pain  of  this  type  and 
distribution  which  may  accompany  a ‘posterior  ulcer  adherent  to 
the  pancreas’,  and  entered  this  as  my  diagnosis  accordingly.  I had 
him  X-rayed  and  the  radiologist  found  a spasmodic  deformity  strongly 
suggesting  a mid-gastric  ulcer.  There  was  no  response  to  medicine 
or  diet.  I therefore  asked  Mr.  L.  Bromley  to  operate.  He  found  a 
posterior  duodenal  ulcer  attached  to  the  pancreas  and  no  gastric 
ulcer.  A gastro-jejimostomy  was  performed.  In  spite  of  his  years  the 
patient  did  well,  after  a stormy  passage,  and  has  remained  fit  subse- 
quently. 

Case  3.  A case  of  aortic  disease  with  abdominal  angina  subjected  to 
alimentary  tract  investigations. 

A man,  aged  55,  with  a history  of  ‘valvular  heart  disease’  first 
recognized  12  years  previously  began  8 years  later  to  experience  a 
‘grinding  pain’  around  the  navel.  This  was  invariably  induced  by 
walking,  especially  up  a slope,  and  it  ‘pulled  him  up*.  He  also  had 
another  pain  shooting  in  character  and  radiating  up  towards  the 
xiphisternum.  This  would  waken  him  between  2 and  4 a.m.,  and  he 
found  that  by  sitting  up  and  eructating  he  obtained  relief.  In  the 
next  year  he  was  very  fully  investigated  from  the  gastro-intestlnal 
point  of  view,  but  the  only  conclusions  transmitted  to  him  were  that 
he  had  colitis  and  a dropped  colon.  No  treatment  for  his  cardio- 
vascular disease  was  prescribed.  I saw  him  a year  later  with  symp- 
toms and  signs  of  commencing  heart-failure.  With  the  onset  of 
dyspnoea  and  general  weakness  the  pain  on  walking  had  disappeared, 
but  the  night  pains  were  more  troublesome.  The  first  pain  was 
undoubtedly  anginal.  The  second  pain,  it  seemed  to  me,  might  well 


so 


TILE  CLINICAL  STUDY  OF  PAIN 
have  a vascular  basis  too  and  be  dependent  on  clianges  affecting 
the  visceral  branches  of  the  abdominal  aorta.  lie  died  within  a few 
months. 

Case  4.  A case  in  ichich  opinions  as  diverse  as  coronary  thrombosis 
and  gall-stones  were  entertained  by  different  observers. 

I was  consulted  by  a man  in  the  fifties  who  gave  me  the  following 
story.  Ten  weeks  previously  he  was  taken  at  lus  work  with  a terrible 
pain  in  the  chest  which  was  ‘one  great  box  of  ache’.  lie  wished  he 
were  dead,  and  for  a time  fainted  with  the  pain,  which  did  not  leave 
him  for  4 hours.  The  pain  had  started  under  the  right  breast,  passed 
across  the  sternum  to  the  left  shoulder  and  down  the  left  arm.  He 
was  seen  in  the  attack  by  a doctor,  who  regarded  the  symptoms  os 
anginal  and  gave  him  amyl  nitrite  and  morpliine  with  little  relief. 
Eventually  he  was  taken  home.  The  pain  did  not  leave  him  till  the 
next  day.  He  was  pyrexial  for  several  days  and  was  seen  by  his  own 
doctor,  who  on  the  strength  of  resistance  and  tenderness,  and  ‘some- 
thing coming  up  against  the  palpating  hand1  under  the  right  rib 
margin,  made  a provisional  diagnosis  of  cholecystitis  and  gall-stones. 
This  doctor  had  the  advantage  of  seeing  him  during  lus  illness  and 
I did  not.  Respecting  each  other’s  opinions  we  have  agreed  to  differ, 
but  perhaps  I may  give  the  further  evidence  on  which  I based  my 
diagnosis  of  coronary  thrombosis.  Firstly,  I ascertained  that  for  a 
year  past,  and  especially  in  cold  weather,  he  had  experienced  an  nolle 
across  the  chest  when  he  walked  after  a meal.  A meal  without  a 
walk  and  a walk  on  an  empty  stomach  did  not  produce  this  effect. 
These  symptoms  bad  been  more  severe  shortly  before  his  grave 
seizure.  Secondly,  since  the  seizure  he  had  found  tliat  he  could  not 
climb  stairs  without  the  old  ache.  Thirdly,  undressing  in  my  presence 
caused  slight  dyspnoea.  Fourthly,  his  heart-sounds  were  faint  and 
equalized  and  his  blood -pressure  was  low  for  his  age  and  type,  105 
systolic,  80  diastolic.  Fifthly,  he  had  had  attacks  of  intermittent 
claudication  and  the  posterior  tibial  artery  was  tliickencd  in  further 
evidence  of  the  existence  of  vascular  disease. 

Conclusion 

It  is  a criticism  sometimes  levelled  at  the  clinician  that 
his  work  is  regrettably  unscientific.  In  general  the  criticism 
may  seem  justified,  and  we  know  well  enough  that  we 
cannot  make  of  bedside  medicine  an  exact  sort  of  science. 
But  in  particular  it  is  indisputable  that  a careful  clinical 
examination  or  inquiry  is  just  as  much  a scientific  pro- 
cedure as  any  other  measure  of  research.  According  to 
Huxley’s  definition,  ‘Science  is  nothing  but  trained  and 
organized  common  sense* — a definition  which  we  should  be 


THE  CLINICAL  STUDY  OF  PAIN  51 

very  ready  to  accept,  and  which  applies  particularly  well 
to  clinical  work. 

We  hear  much  talk  at  the  present  day  of  research  in 
general  practice.  I marvel  at  the  temerity  of  anyone  who 
can  suggest  that  the  busy  practitioner  should  add  another 
burden  to  his  arduous  life;  but  if  there  is  oneway  of  research 
not  involving  too  great  a consumption  of  time,  and  open 
alike  to  the  general  practitioner  or  to  any  other  branch  of 
the  profession,  it  is  that  of  keeping  very  full  clinical  notes 
on  selected  cases  with  a view  to  the  solution  of  a selected 
problem  in  symptomatology.  No  symptoms  better  lend 
themselves  to  such  a process  of  inquiry  than  some  of  the 
common  pains  of  daily  practice.  A series  of  cases  of  head- 
ache, backache,  or  abdominal  pain,  as  fully  investigated  as 
circumstances  will  permit,  and  carefully  followed  through 
the  years,  will  certainly  provide  individual  rewards  for  their 
investigator,  and  may  ultimately  furnish  the  material  for 
a reasoned  contribution  to  morbid  physiology.  System  and 
patience  are  necessary,  together  with  an  inquiring  mind. 
The  only  essential  apparatus  for  the  research  is  a good  card 
index. 


IV 

VISCERAL  PAIN  AND  REFERRED  PAIN1 

There  are  problems  in  medicine  which  make  a general 
appeal,  and  others  of  a more  special  character  which  cannot 
equally  attract  all  minds.  In  choosing  for  discussion  certain 
aspects  of  pain,  I have  hoped  at  least  to  avoid  the  imputa- 
tion of  specialism,  for  it  would  be  difficult  to  conceive  a 
problem  more  universal  and  more  appropriate  to  our  art. 
Whether  our  inclinations  be  medical  or  surgical,  or  our 
thoughts  cast  in  a physiological  or  an  anatomical  mould ; 
whether  our  work  be  academic  or  more  severely  practical, 
there  are  features  of  the  problem  which  can  hardly  fail 
to  claim  attention.  To  seek  out  the  causes,  to  assess  the 
consequences,  and  to  encompass  the  relief  of  pains  is  for 
most  of  us  a daily  duty.  Familiarity  cannot— or  should  not 
— deprive  the  subject  of  its  fascination  or  blind  us  to  its 
difficulties. 

If  there  is  a fault  in  us  bred  of  familiarity  it  is,  I believe, 
the  old  fault  of  omitting  to  probe  sufficiently  deeply  into 
causes ; the  fault  of  accepting  the  fact  of  common  symptoms 
without  trying  to  explain  them.  F or  this  reason  my  remarks 
will  be  confined  to  a review  of  the  present  state  of  our  know- 
ledge of  the  nature  and  causes  of  some  more  familiar  types 
of  pain.  Research  into  the  subject  does  not  commend  itself 
to  the  experimentalist  in  the  laboratory,  for  subjective 
phenomena  are  difficult  to  pursue  in  animals,  and  the  varie- 
ties of  pain  which  can  be  reproduced  and  studied  in  the 
healthy  human  being  are  of  necessity  limited.  On  the  other 
hand,  those  who  are  engaged  in  the  practice  of  medicine 
or  surgery,  and  have  the  most  frequent  opportunities  of 
observing  the  experiments  in  pain  with  which  Nature  herself 
provides  us,  are  usually  so  harassed  by  the  exigencies  of 
work  that  ordered  observations  are  hard  to  accumulate  and 
still  more  hard  to  analyse.  Furthermore,  the  experiments 
often  take  months  or  years  to  march  to  their  conclusion, 

1 Lancet,  1020,  L 60S. 


S3 


VISCERAL  PAIN  AND  REFERRED  PAIN 
and  only  too  frequently  they  are  not  concluded  at  all.  I 
think,  however,  it  may  fairly  be  urged  that  we  owe — as  we 
should  do-— our  most  valuable  information  relating  to  the 
mechanism  and  distribution  of  pains  to  the  clinicians,  and 
that  it  should  rest  with  them  to  direct  inquiries  in  the 
future,  employing  ever  more  careful  methods,  and  seeking 
scientific  co-operation  whenever  possible.  With  the  work 
of  such  men  as  John  Hilton,  James  Mackenzie,  and  Henry 
Head  to  reflect  upon  we  do  not  lack  for  inspiration  in  this 
country. 

It  is  with  some  diffidence  that  I approach  the  subject  of 
local  pain  and  referred  pain  in  visceral  disease,  for  if  the 
more  superficial  pains  are  difficult  to  elucidate  the  deeply 
seated  pains  are  more  so.  Moreover,  the  ground  which 
must  be  covered  is  wide  and  beset  with  controversies.  I 
shall  confine  myself  to  a consideration  of  pain  associated 
with  disease  of  the  hollow  viscera,  for  it  is  doubtful  whether 
the  solid  viscera  are  possessed  of  any  sensibility.  My  argu- 
ment will  be  mainly  clinical,  and  I must  pray  the  physio- 
logists and  anatomists  for  leniency  whenever  my  remarks 
seem  to  lack  that  precision  which  their  more  ordered  sciences 
demand. 


The  Mechanism  of  Visceral  Pain 
To  begin  with,  let  me  recall  that  there  have  been  two 
main  schools  of  thought  in  regard  to  the  mechanism  of  a 
visceral  pain.  The  first  school,  basing  its  views  on  the 
work  of  Lennander  [1]  and  having  the  late  Sir  James 
Mackenzie  [2]  as  its  most  vigorous  protagonist,  concludes 
that  pain  is  not  felt  in  the  viscera,  but  that  it  is  referred  to 
the  somatic  tissues  supplied  by  the  same  segment  of  the 
cord  which  supplies  the  viscus  in  question.  The  latest  edi- 
tion of  a well-known  physiology  text-book  still  perpetuates 
this  view.  The  second  school,  supported  by  Ross  [8]  and 
Hurst  [4]  and  perhaps  the  majority  of  physicians,  while 
recognizing  that  visceral  disease  may  be  accompanied  by 
referred  somatic  pain,  contends  that  the  viscera  themselves 
are  capable  of  feeling  pain  in  the  presence  of  appropriate 
stimuli. 


1.  That  there  is  a true  visceral  pain  felt  by  the  viscus. 

2.  That  visceral  pain  is  commonly  due  to  an  abnormal 
increase  in  the  tension  of  the  muscular  element  of 
the  wall  of  the  viscus,  this  increased  tension  resulting 
either  from  contraction  or  from  a failure  on  the  part 
of  the  muscle-fibre  to  relax  adequately  in  the  presence 
of  increased  intravisceral  pressures. 

3.  That  visceral  pain  when  occurring  alone,  or  dissociable 
from  attendant  somatic  pains,  may  be  accurately 
localized  by  the  patient. 

4.  That  referred  somatic  pain  and  tenderness — e.g.,  the 
viscero-sensory  reflexes — and  the  associated  viscero- 
motor reflexes,  although  they  may  accompany  a severe 
visceral  crisis  of  mechanical  origin,  more  frequently 
express  an  inflammatory  lesion  of  the  viscus. 

5.  That,  when  persistent,  they  invariably  express  organic 
disease  of  the  viscus  of  an  inflammatory  kind. 

I shall  illustrate  my  remarks  by  referring  to  painful  dis- 
orders of  the  stomach,  the  gall-bladder,  the  appendix,  the 
intestine,  the  kidney  and  ureter,  the  uterus  and  Fallopian 
tubes. 

Normal  Sensibility  of  Hollozc  Organs 

If  it  be  claimed  that  visceral  pain  is  not  produced  in  the 
viscus  it  seems  pertinent  to  inquire  where  the  normal  sensa- 
tions peculiar  to  certain  viscera  are  felt.  I have  never  seen 
it  suggested  that  these  normal  sensations  are  referred  to 
the  somatic  tissues,  nor  does  daily  experience  suggest  that 
they  are  felt  elsewhere  than  in  the  viscus.  The  heart  and 
aorta,  excepting  for  the  sensations  of  praecordial  fullness 
and  retrosternal  oppression  experienced  during  violent  effort 
or  emotion,  may  be  said  to  be  insensitive  under  physio- 
logical conditions.  In  the  case  of  the  stomach  we  recognize 
the  gastric  elements  of  the  appetite  and  hunger  sensations, 
and  the  sensations  of  fullness  or  repletion.  These  have  been 
clearly  related  with  the  tonic  and  peristaltic  activity  of  the 
stomach  wall,  and  the  work  of  Carlson  [5]  and  Hurst  [4] 
would  seem  to  indicate  that  the  sensations  depend  on  the 


VISCERAL  PAIN  AND  REFERRED  PAIN  55 

state  of  tension  in  the  gastric  muscle-fibre.  Of  the  appendix 
and  gall-bladder  we  are  quite  unaware  in  health.  Of  the 
intestine  we  are  aware  whenever  local  distension  with  flatus 
occurs.  The  rectum  clearly  appreciates  states  of  fullness, 
at  times  of  urgency  amounting  to  pain,  and  most  of  us 
would  agree  that  its  sensations  are  deeply  and  not  super- 
ficially situated.  The  sensation  of  the  desire  to  micturate  is 
felt  in  the  urethra  and  in  the  bladder  also  when  it  is  over- 
distended. All  these  physiological  sensations  are  related  to 
increasing  pressure  on  the  walls  of  the  viscus  and  are  re- 
lieved by  evacuation.  Menstrual  pains  are  felt  locally,  but 
are  frequently  accompanied  by  a more  superficial  sacral 
pain.  It  is,  however,  worthy  of  note  that  a state  of  conges- 
tion akin  to  the  effects  of  inflammation  is  present  in  this 
condition  in  addition  to  increased  muscle  tension,  and  that 
no  equivalent  congestion  is  present  during  the  normal 
functional  activity  of  other  hollow  viscera. 

Lennander  [I]  showed  that  the  abdominal  viscera  when 
exposed  could  be  pricked,  pinched,  cut,  or  burnt  without 
causing  pain,  and  we  are  all  familiar  with  the  insensibility 
to  these  stimuli  of  a colotomy  loop.  Waugh  [6]  has  shown 
a similar  insensibility  in  the  case  of  the  heart.  It  is  further 
obvious  that  the  gastric  and  intestinal  mucosa  have  no 
tactile  and  very  little  thermal  sensibility,  for  if  they  had, 
we  should  be  far  more  conscious  of  ingested  foods  and  fluids, 
of  enemata,  and  of  the  normal  processes  of  digestion.  Hurst 
[4]  and  his  collaborators  demonstrated  by  experiment  the 
insensibility  of  the  gastric  and  rectal  mucosa  to  tactile, 
thermal,  and  chemical  stimuli,  and  Hilton  [7]  long  ago 
remarked  on  the  insensibility  of  the  rectal  as  compared  with 
the  anal  mucosa.  These  observations  support  the  conten- 
tion that,  if  the  hollow  viscera  are  sensitive,  it  is  not  their 
serous  or  mucous  coats  hut  their  muscular  coats  which 
appreciate  the  sensations.  Those  who  contend  that  the 
viscera  are  insensitive  seem  to  have  paid  too  little  regard 
to  the  fact  that  special  organs  respond  only  to  special 
stimuli.  Thus  the  eye  appreciates  light  and  not  sound ; the 
skin  appreciates  touch,  temperature,  and  traumatic  pains, 
all  of  which  it  is  physiologically  essential  for  it  to  appreciate ; 


50  VISCERAL  PAIN  AND  REFERRED  PAIN 

the  skeletal  muscles  appreciate  position  and  tension  and  the 
strength  of  opposing  forces  and  (in  states  of  extreme  tension) 
pain,  but  they  arc  not,  I believe,  sensitive  to  cutting,  prick- 
ing, or  burning.  There  is  no  reason  for  the  hollow  viscera 
below  the  gullet  to  appreciate  tactile  or  thermal  stimuli,  but 
it  is  vi  tally  necessary  for  them  to  appreciate  states  of  fullness 
and  emptiness.  By  analogy  it  seems  reasonable  to  insist  that 
the  plain  muscle  of  the  hollow  viscera  is  endowed  with 
the  same  sensibility,  positive  and  negative,  as  the  skeletal 
muscles ; in  other  words,  that  visceral  sense  is  muscle-sense. 
The  sensations  of  fullness  or  emptiness  are  thus  parallel  with 
the  sensations  of  posture  and  tension  in  a limb.  Pain 
(whether  in  skeletal  or  plain  muscle)  results  when  tension  is 
greatly  exaggerated  in  one  manner  or  another.  The  common 
factor  present  in  all  cases  of  visceral  pain  is  an  increase 
in  muscular  tension  or,  perhaps  (to  conform  with  Lewis’s 
work  on  angina),  the  ischaemia,  and  the  associated  chemical 
changes  accompanying  an  increase  in  tension.  The  reliev- 
ing factor,  whether  it  be  the  passage  of  a gall-stone  in 
biliary  colic  or  the  ingestion  of  food  in  hunger  pain,  is  a 
factor  which  reduces  tension  in  the  wall  of  the  viscus. 

What  further  evidence  have  we  that  -visceral  pain  is 
deeply  felt  and  not  somatic  ? It  will  be  agreed  that  ordinary 
stomach-ache  and  intestinal  colic  give  the  impression  of 
being  felt  internally.  Those  who  have  experienced  severe 
visceral  pains  of  mechanical  origin,  such  as  renal  and  biliary 
colic,  are  agreed  that  these  sensations  seem  to  be  deep  to 
the  body  wall.  I think  it  is  also  true  that  the  majority  of 
non-inflnmmatory  visceral  pains  (unless  they  fall  into  the 
group  of  the  severe  visceral  crises)  are  but  rarely  accom- 
panied by  reflected  superficial  pain  or  soreness,  and  in  the 
case  of  inflammatory  lesions  we  may  observe,  as  I shall 
show,  referred  somatic  pain  or  tenderness  occurring  in  the 
absence  of  local  visceral  pain,  and  thus  suggesting  that  the 
causal  processes  are  not  identical. 

Guarded  though  we  should  be  in  accepting  the  observa- 
tions of  our  patients  as  accurate  evidence,  we  must,  never- 
theless, attach  importance  to  certain  ‘gestures’  which  they 
employ  in  indicating  the  seat  of  their  pain.  These  gestures 


VISCERAL  PAIN  AND  REFERRED  PAIN  57 

do  not,  as  a rule,  apply  to  a somatic  segment,  but  to  the 
surface-marking  of  the  viscus.  Thus,  in  describing  anginal 
pain  the  patient  places  his  clenched  hand  to  the  sternum  as 
though  to  indicate  a median  or  cardiac  origin  for  his  pain, 
and,  perhaps,  incidentally,  to  imply  its  gripping  character. 
The  pain  of  gastric  ulcer  is  indicated  with  the  tips  of  two  ) 
or  three  fingers  applied  to  the  mid-epigastric  point  or  occa-  j 
sionally  just  to  the  left  of  this  point ; the  pain  of  duodenal  \ 
ulcer  by  a similar  demonstration  frequently  just  to  the  ' 
right  of  the  mid-line.  The  gesture  of  renal  colic  is  made 
familiar  by  the  pictorial  advertisements  of  a certain  proprie- 
tary back-ache  pill ; the  hand  grasps  the  loin  usually  with 
the  fingers  over  the  back  and  thumb  in  front,  as  though 
to  imply  that  the  pain  requiring  subjection  is  rather  more 
posterior  than  anterior  and  deeply  situated  in  the  actual 
position  which  the  kidney  occupies.  The  localization  of 
pain  in  gall-bladder  and  appendicular  disease  (when  there 
is  no  confusion  due  to  associated  inflammation  or  gastric 
and  intestinal  disturbance)  is  remarkably  accurate.  The 
position  of  a calculus  impacted  in  the  ureter  may  also  be 
accurately  shown  when  distraction  by  concurrent  renal 
colic  or  other  symptoms  is  not  too  strong.  Intestinal  pains 
are  less  easily  localized,  but  here  the  actual  position  of 
the  painful  contraction  is  variable,  for  intestinal  colic  is 
not  confined  to  one  spot  as  is  the  case  with  biliary  or  renal 
colic.  Small  intestine  pains  are  usually  felt  around  the 
navel,  and  colonic  pains  between  the  navel  and  the  sym- 
physis pubis.  When,  however,  obstruction  occurs  at  a more 
or  less  fixed  point,  such  as  the  hepatic,  splenic,  or  sigmoid 
flexures,  then  the  localization  is  commonly  precise.  One  of 
the  most  recent  text-books  of  physiology,  in  the  very  brief 
references  to  this  subject  which  it  makes,  asserts  that  vis- 
ceral pain  is  vaguely  and  inconstantly  localized.  I believe 
that  clinical  experience  teaches  otherwise,  if  only  we  are 
careful  to  dissociate  the  primary  or  local  from  the  secondary 
and  referred  phenomena. 

It  will  be  conceded  that  the  reflected  phenomena  of 
visceral  disease  are  best  demonstrated  in  association  with 
the  very  severe  forms  of  visceral  pain  or  in  association  with 


58  VISCERAL  PAIN  AND  REFERRED  TAIN 

inflammatory  disease.  The  arm  pain  of  angina,  the  sub- 
scapular  pain  of  cholelithiasis,  and  the  testicular  pain  in 
ureteric  colic  are  the  classical  examples  of  the  former  group ; 
of  the  latter  the  cutaneous  hyperalgesia  and  muscular 
guarding  found  in  appendicitis  or  in  relation  to  a chronic 
gastric  ulcer  arc  the  best  examples.  It  is  worthy  of  note 
that  these  reflected  phenomena  rarely  accompany  visceral 
disease  of  a functional  kind;  in  other  words,  that  they  arc 
generally  associated  with  local  organic  changes.  In  stomach- 
ache due  to  extragastric  causes  I have  not  found  cutaneous 
soreness  or  muscular  guarding.  With  the  subscapular  pains 
of  gall-stones  it  may  be  pleaded  that  the  pain  is  as  much 
an  effect  of  the  cholecystitis  ns  of  the  stones ; certainly  an 
identical  subscapular  pain  occurs  in  cholecystitis  without 
gall-stones.  In  the  testicular  pain  of  calculous  ureteric  colic 
the  ureteric  mucosa  must  frequently  be  ulcerated  or  in- 
flamed and  testicular  pain  may  occur  without  any  attack 
of  ‘colic’.  It  is  upon  observations  of  this  kind  that  we  may 
base  the  conclusion  that  visceral  pain  expresses  a perturba- 
tion of  visceral  function  (ichich  may  or  may  not  be  due  to  local 
organic  disease),  tchile  the  somatic  phenomena  generally  ex- 
press a structural  lesion  of  the  trail  of  the  viscus. 

Gastric  Pain 

My  interest  in  the  subject  of  visceral  and  referred  pain 
was  first  stimulated  by  studying  cases  of  gastric  and  duo- 
denal ulcer.  The  pain  of  duodenal  ulcer,  usually  gnawing  or 
aching  or  described  as  a feeling  of  great  pressure,  occurs 
when  the  stomach  is  in  the  posture  of  approaching  empti- 
ness, but,  through  reflexly  enhanced  tonic  action,  its  muscle 
becomes  and  remains  abnormally  taut.  This  pain  is  relieved 
when  the  stomach  adapts  its  posture  or  relaxes  to  accom- 
modate introduced  food  or  fluid,  or  when  the  ‘resistance* 
is  withdrawn  and  intragastric  pressure  reduced  by  complete 
emptying.  The  pain  of  gastric  ulcer  occurs  when  the  tension 
in  certain  muscle- fibres,  reflexly  tautened  or  structurally 
shortened  by  the  ulcer,  is  further  augmented  by  the  intro- 
duction of  food.  In  cases  of  ulcer  we  are  frequently  told  by 
the  patient  that  these  spontaneous  pains  are  accompanied 


VISCERAL  PAIN  AND  REFERRED  PAIN  59 

and  often  followed  by  local  epigastric  soreness  or  hyper- 
algesia. In  a large  proportion  of  cases  we  discover  deep 
somatic  tenderness.  In  a much  smaller  proportion  we  find 
superficial  and  deep  hyperalgesia  (or  soreness)  of  the  skin, 
together  with  muscular  guarding  of  one  or  other  rectus  and 
exaggeration  of  the  abdominal  reflex  on  one  side.  These 
signs  are  more  likely  to  be  demonstrable  if  the  patient  has 
recently  had  an  attack  of  pain  or  is  in  pain  at  the  time 
of  the  examination.  On  the  other  hand,  these  signs  may 
persist  for  days  after  the  subsidence  of  all  spontaneous  pain 
as  the  result  of  appropriate  treatment  in  bed,  and  they  may 
not  finally  disappear  for  a week  or  fortnight.  The  purpose 
of  these  reflexes  is  surely  protective,  so  why  should  they 
only  be  present  when  spontaneous  pain  is  present  ? They 
disappear  completely  when  the  ulcer  is  healed,  as  judged  by 
the  disappearance  of  occult  blood  from  the  stools,  and  they 
are  not  present  in  cases  of  established  pyloric  stenosis.  They 
are,  therefore,  probably  due  to  stimuli  constantly  passing 
from  the  ulcerated  area  to  the  cord,  and,  although  they  may 
be  brought  to  light  or  reinforced  by  them,  are  not  directly 
attributable  to  the  painful  contractions  in  the  stomach  wall 
which  cause  the  visceral  or  deeply  seated  pain.  These  reflex 
signs  are  more  constantly  present  with  the  deeper  and  more 
chronic  ulcers  which  invade  the  muscular  coat.  Although 
the  pain  of  cancer  of  the  stomach  may  equal  or  surpass  in 
severity  the  pains  of  gastric  ulcer,  it  is  much  more  rarely 
accompanied  by  somatic  signs.  Thus,  while  it  is  difficult 
to  palpate  deeply  in  many  ulcer  eases  on  account  of  somatic 
tenderness  and  muscular  guarding,  in  cancer  the  muscles 
are  often  relaxed  and  the  tumour  can  be  felt  without  causing 
flinching  or  pain.  I believe  this  apparent  discrepancy  may 
be  related  to  the  fact  that  simple  ulcers  erode  and  de- 
stroy the  muscle-fibres  in  which  the  nerve-endings  ramify, 
whereas  the  growth  merely  infiltrates  between  the  fibres — 
an  histological  distinction  which  is  regarded  as  of  diagnostic 
import  by  pathologists  when  considering  the  nature  of 
large  chronic  ulcers.  When  ‘guarding*  is  present  in  cancer 
of  the  stomach  it  is  usually  bilateral  and  evidence  of  peri- 
toneal involvement;  in  gastric  ulcer  it  is  usually  left-sided. 


CO  VISCERAL  PAIN  AND  REFERRED  PAIN 

and  in  duodenal  ulcer  right-sided.  Pain  is  referred  to  the 
back  over  the  lower  ribs,  particularly  in  the  case  of  posterior 
ulcers  eroding  the  pancreas.  Somatic  signs  arc  rarely  present 
in  simple  gastritis,  because  the  lesion  is  too  superficial  and 
does  not  involve  the  muscular  layer.  The  following  cases 
illustrate  some  of  the  points  to  which  I have  referred. 

Case  1.  J.  D.,  male,  aged  about  50,  was  diagnosed  clinically  and 
with  the  aid  of  X-rays,  test-meal,  and  the  presence  of  occult  blood 
in  the  stools  os  having  a duodenal  ulcer.  On  admission  to  the  ward 
he  had  deep  cutaneous  soreness,  deep  tenderness  over  the  right  upper 
rectus,  and  the  abdominal  reflex  was  exaggerated  in  the  right  upper 
quadrant.  The  deep  soreness  was  very  marked  and  at  times  super- 
ficial soreness  was  also  present,  the  patient  volunteering  the  state- 
ment that  the  weight  of  a book  as  he  read  in  bed  and  even  tliat  of 
the  bed-clothes  was  sometimes  insupportable.  The  signs  persisted 
for  some  time  after  he  lost  his  pain,  but  then  gradually  became  less 
and  less  distinct.  Deep  tenderness  was  the  last  sign  to  disappear,  and 
its  complete  disappearance  coincided  tcith  the  return  of  negative  occult 
blood  reports  from  the  clinical  laboratory. 

Case  2.  A young  man,  aged  27,  was  diagnosed  as  having  a gastric 
ulcer  at  out-patients  and  the  X-ray  report  confirmed,  stating  that 
there  was  a penetrating  ulcer  of  the  lesser  curvature.  On  his  first 
attendance  he  was  free  from  pain  and  the  only  sign  demonstrable 
was  deep  mid-line  tenderness  in  the  epigastrium.  On  his  next  visit 
he  was  actually  in  pain,  and  he  showed,  in  addition  to  the  mid-line 
tenderness,  deep  cutaneous  soreness  in  the  mid-line,  left-sided  exag- 
geration of  the  abdominal  reflex,  and  left-sided  guarding. 

It  is  very  rare  in  my  experience  for  superficial  soreness, 
elicited  with  the  head  of  a pin  as  Head  [8]  described,  to 
be  present  in  gastric  disease.  In  distinguishing  between  a 
gastric  and  a duodenal  ulcer  the  horizontal  level  of  tender- 
ness is  less  reliable  than  the  right-  or  left-sidedness  of  the 
viscero-sensory  and  viscero-motor  signs. 

Pain  in  Gall-bladdek  and  Bile -ducts 

The  pain  of  biliary  colic  is  referred  to  the  gall-bladder 
point,  corresponding  with  the  ninth  costal  cartilage,  or 
sometimes  more  centrally  below  the  xiphistemum.  It  is 
almost  invariably  a crescendo  pain.  It  is  often  difficult  to 
dissociate  the  attendant  gastric  pain  from  the  true  gall- 
bladder pain.  In  association  with  gall-stones  and  chronic 
cholecystitis  it  is  not  uncommon  to  find  a recurrent  gastric 


VISCERAL  PAIN  AND  REFERRED  PAIN  61 

pain,  often  -worse  at  night,  simulating  the  pain  of  ulcer 
and  dependent  upon  similar  reflex  disturbances  of  gastric 
motility.  The  viscero-sensory  accompaniments  of  chole- 
cystitis— whether  occurring  with  or  without  gall-stones — 
include  superficial  and  deep  soreness  in  the  right  upper 
quadrant  of  the  abdomen,  right  subscapular  and  inter- 
scapular  pains,  and  tenderness  over  the  middle  dorsal 
spines  and  along  the  course  of  the  eleventh  right  rib. 
Muscular  guarding,  amounting  in  acute  cases  to  actual 
rigidity,  may  also  be  present,  and,  in  subacute  cases, 
exaggeration  of  the  abdominal  reflex  on  the  right  side. 
‘Shoulder  pain’,  so  often  referred  to  as  a sign  of  gall-stones, 
should  be  reserved  for  the  description  of  pain  referred  along 
the  phrenic  nerve  to  the  C4  area  in  eases  of  inflammation 
involving  the  under  surface  of  the  diaphragm  or  in  dia- 
phragmatic pleurisy.  It  is  best  seen  in  liver  abscess  and 
subphrenic  abscess  and  is  sometimes  an  early  symptom  of 
a perforating  gastric  ulcer.  I have  never  met  with  it  in  un- 
complicated gall-stones  or  cholecystitis.  I shall  here  give 
the  notes  of  one  case  only,  that  of  a medical  man,  who  helped 
me  with  careful  observations. 

Case  3.  The  patient  first  came  under  observation  on  account  of 
severe  attacks  of  epigastric  pain  of  unexplained  causation.  At  the 
time  of  investigation  he  was  free  from  all  symptoms.  A week  spent 
in  thorough  investigation  by  the  various  modem  methods  failed  to 
clear  up  the  diagnosis.  The  only  positive  sign  teas  slight  tenderness  over 
the  fifth  and  sixth  dorsal  spines,  and  the  possibility  of  gall-stones  was  on 
this  account  considered.  A few  weeks  later  I saw  him  in  an  attack 
with  a palpable  gall-bladder  and,  on  the  following  day,  a rigid  right 
Upper  rectus  and  friction  sounds  below  the  rib  margin.  At  operation 
a very  much  thickened  and  inflamed  gall-bladder  filled  with  stones 
was  found.  Some  months  after  the  operation  he  had  one  further 
attack  of  biliary  colic,  perhaps  due  to  n stone  left  in  the  dilated  duct. 
Later  still  I saw  liim  with  troublesome  referred  pains  in  the  mid- 
dorsal region  unaccompanied  by  abdominal  colic  or  epigastric  pain. 

I thought  that  these  pains  were  due  to  persisting  infection  in  the 
dilated  ducts,  and  with  hexamine  the  symptoms  were  at  first  relieved. 
Later,  however,  they  recurred  and  hexamine  failed  to  bring  relief. 
The  patient  has  since  written  to  me  in  the  following  words : ‘One  day 
it  occurred  to  me  that  this  pain  was  purely  a dragging  pain  and  might 
be  due  to  inability  of  the  liver  to  get  rid  of  its  secretions  through  a 
kinked  duct.  I decided  to  sleep  on  my  left  side.  I could  not  do  this 


02  VISCERAL  PAIN  AND  REFERRED  PAIN 

before,  but  the  difficulty  was  overcome.  The  effect  was  excellent.  I 
never  get  that  pnin  now  unless  I happen  to  turn  on  my  right  side, 
then  It  comes  next  day.  I have  tried  the  trick  again  and  again  and 
there  can  be  no  doubt  of  cause  and  effect. . . 

It  is  difficult  in  this  ease  to  decide  how  far  the  referred 
phenomena  should  be  regarded  as  an  effect  of  inflammation 
and  how  far  as  an  effect  of  mechanical  distention  of  the  ducts. 
In  the  first  instance  they  were  seemingly  relieved,  as  I have 
seen  them  relieved  in  other  cases,  by  treatment  directed 
towards  disinfection  of  the  biliary  tract.  Latterly  they  were 
relieved  by  a simple  expedient  likely  to  facilitate  evacuation 
of  the  duct.  Perhaps  it  is  fair  to  suggest  that  both  factors 
played  their  part,  just  ns  mechanical  and  inflammatory 
factors  are  shown  to  buttress  one  another  in  promoting  the 
somatic  signs  of  gastric  ulcer.  Hilton  [7]  was  the  first  to 
give  an  anatomical  explanation  for  the  frequent  association 
of  subscapular  and  intcrscapular  pain  with  diseases  of  the 
upper  alimentary  tract,  pointing  out  the  connexions  be- 
tween the  nerve  supply  to  the  stomach,  liver,  duodenum, 
and  pancreas  (great  splanchnic  and  solar  plexus),  and  the 
fourth,  fifth,  and  sixth  dorsal  nerves. 

Appendicular  Pain 

Among  the  varieties  of  disease  collected  under  the  heading 
of  acute  appendicitis  there  are  two  broad  clinical  types 
which  it  is  essential  to  distinguish.  The  first  is  the  ‘inflam- 
matory type’  in  which,  following  upon  infection  of  the 
mucosa  or  submucosa,  there  develops  general  redness  and 
inflammation  of  the  organ  with  or  without  obvious  pus 
formation.  In  this  type,  in  addition  to  visceral  pain, 
cutaneous  hyperalgesia,  muscular  guarding  or  rigidity,  and 
pyrexia  are  commonly  present.  If  reflex  signs  are  carefully 
sought  for  they  may  be  found  in  some  of  the  mildest  and 
earliest  cases  in  which  it  might  otherwise  be  difficult  to 
arrive  at  a diagnosis.  The  second  type  is  the  ‘gangrenous’ 
appendix,  which  may  give  rise  at  first  to  exceedingly  severe 
visceral  pain,  but  not  infrequently  with  a complete  or 
almost  complete  absence  of  somatic  signs  and  pyrexia.  In 
the  absence  of  these  signs  the  diagnosis  is  sometimes  un- 


VISCERAL  PAIN  AND  REFERRED  PAIN  03 

happily  postponed,  and  yet  it  is  the  type  above  ail  others 
in  which  early  operation  is  imperative.  In  either  type  there 
may  be  a sudden  disappearance  of  the  visceral  pain  when 
the  appendix  ruptures — a strong  point  in  support  of 
the  contention  that  visceral  pain  is  an  effect  of  increased 
tension.  In  the  gangrenous  type  we  have  a lesion  in  which 
not  only  the  lumen  but  also  the  circulation  of  the  organ  has 
become  obstructed.  Possibly  the  absence  or  paucity  of 
somatic  signs  in  these  cases  may  be  explained  by  the 
mechanical  nature  of  the  lesion  in  the  early  stages  and  by 
the  ischaemia  of  the  tissues  involved  in  the  later  stages. 

Case  4.  A medical  student,  aged  22,  came  to  me  some  years  ago 
with  the  following  history:  Three  montlis  previously  he  had  had  a 
sudden  attack  of  pain  in  the  epigastrium  which  later  settled  into  the 
lower  abdomen.  He  stated  that  there  was  tenderness  on  the  right  side 
and  round  the  navel,  that  he  vomited,  and  that  his  temperature  rose 
to  09-4°  F.  Forty-eight  hours  later  he  was  quite  well.  He  remained 
fit  for  a month  and  then  had  a similar  attack  in  which  there  was  pain 
and  tenderness  in  the  epigastrium.  Ten  days  before  he  saw  me  he 
had  had  a third  attack  which  started  absolutely  abruptly  at  3 p.m., 
with  pain  in  the  epigastrium  which  doubled  him  up  and  made  him 
feel  cold.  At  10  p.m.  the  pain  departed  with  absolute  suddenness 
under  the  following  circumstances.  He  was  on  his  way  home  to  his 
rooms  and  met  a registrar  from  the  hospital  who  told  him  how  ill  he 
was  looking.  He  said : ‘Yes,  I have  a bad  stomach-ache.  . . . No,  I 
have  not,  it  has  gone.’  At  no  time  had  the  pain  been  referred  to  the 
back,  or  groin,  or  testicle.  Between  the  attacks  he  was  perfectly  fit 
in  every  way,  and  at  the  time  of  his  visit  to  me  he  was  quite  free  from 
Bymptoms.  My  physical  overhaul  was  completely  negative  except 
for  showing  local  deep  tenderness  at  McBurncy’s  point.  A radio- 
graphic examination  of  his  alimentary  and  urinary  tracts  was  nega- 
tive. Bastedo's  test  produced  no  localized  pain.  A week  later  all 
tenderness  had  disappeared  and  he  felt  perfectly  well.  I regarded  the 
attacks  as  probably  appendicular,  and  told  him  that  at  the  first  sign 
of  any  recurrence  he  was  to  come  up  to  the  hospital.  As  it  liappened 
the  next  attack  started  in  the  middle  of  the  night,  the  pain  was  of 
great  severity,  and  he  could  not  attract  the  attention  of  anyone  in 
the  house.  He  came  to  see  me  in  the  morning  looking  pale  and  ill. 
There  was  no  pyrexia,  no  cutaneous  soreness,  no  rigidity,  and  only 
very  slight  tenderness  in  the  right  iliac  fossa;  the  pulse  was  not 
accelerated,  but  as  he  lay  on  my  couch  he  preferred  to  do  so  with  the 
right  knee  drawn  up.  I had  him  admitted  to  hospital  at  once,  and 
Mr.  R.  P.  Rowlands  removed  a black  gangrenous  appendix.  At  its 
proximal  end  there  was  a small  thorn  impacted  in  the  lumen  of  the 


Cl  VISCERAL  PAIN  AND  REFERRED  PAIN 

organ.  Although  appendicular  disease  seemed  more  probable,  the 
curiously  abrupt  onset  and  departure  of  pain  in  the  early  attacks  and 
their  epigastric  reference  had  made  me  consider  the  alternative  pos- 
sibility of  one  of  the  major  colics.  With  such  a history  before  me 
now  I should  not  dare  to  await  events. 

Intestinal  Pain 

Intestinal  pains  are  generally  griping  and  rhythmically 
recurrent,  but  with  partially  obstructive  lesions  in  the  large 
bowel  the  pain  may  be  more  sustained.  Excepting  with 
ulcerative  or  inflammatory  lesions  it  is  unusual  to  find 
cutaneous  soreness  or  muscular  guarding  in  intestinal 
disease.  These  signs  may  be  present  with  tuberculous 
ulceration  of  the  ileocaecal  region  and  with  diverticulitis 
of  the  colon,  but  they  are  rare  in  mechanical  obstructions 
and  in  cancer.  Head  [9]  points  out  that  they  may  be  present 
in  typhoid  fever,  but  are  absent  in  lead  colic,  yet  another 
observation  in  favour  of  the  suggestion  that  visceral  pain 
is  an  effect  of  muscular  tension,  while  for  referred  pain  or 
tenderness  the  added  effect  of  inflammation  is  necessary'. 

Renal  and  Uhetehic  Pain 

One  of  my  most  instructive  lessons  in  visceral  pain  and 
referred  pain  was  provided  by  a personal  experience  of 
renal  colic.  I must  apologize  for  referring  to  this  experience 
and  should  hesitate  to  do  so  did  I not  believe  that  personal 
records  by  medical  men  have  a certain  value  of  their  own. 

Cast.  5.  In  February  1022  I began  to  have  attacks  of  left-sided 
renal  colic  and  between  then  and  July  of  the  same  year,  when  I 
passed  a small  calculus,  I had  four  or  five  major  attacks  and  about  a 
dozen  minor  ones.  I was  satisfied  that  both  the  renal  pain,  which 
was  always  crescendo  in  character,  and  later  the  ureteric  pain  were 
deeply  situated.  At  an  intermediate  stage  the  latter  appeared  to  me 
to  be  just  deep  to  the  sacro-iliac  joint,  but  shortly  before  the  stone 
passed  into  the  bladder  it  was  felt  low  down  in  the  left  iliac  fossa. 
One  bad  attack  was  relieved  by  morphine  and  atropine  when  mor- 
phine alone  had  failed.  I was  told  by  a colleague  that  my  loin  muscles 
after  attacks  of  renal  pain  were  hard  on  the  affected  side  and  they 
certainly  remained  tender  for  a day  or  two,  after  the  manner  of  n 
muscle  which  has  been  over-used.  Jolting  and  gentle  thumping  of  the 
loin  were  painful,  but  deep  palpation  caused  no  discomfort.  At  no 
time  did  I discover  any  cutaneous  hyperalgesia.  There  was  frequent 


VISCERAL  PAIN  AND  REFERRED  PAIN  G5 
referred  pain  into  the  left  testicle  during  the  long  period  in  « hieli  the 
stone  was  lodged  in  the  lower  end  of  the  ureter,  and  this  occurred 
quite  independently  of  ureteric  or  renal  crises.  There  were  several 
bouts  of  haematuria,  and  red  cells  and  latterly  leucocytes  were  always 
present  in  the  urine  when  examined.  It  seemed  to  me  that  the 
referred  testicular  pain  was  an  effect  of  local  ulceration  of  the  ureter, 
although  its  intermittency  suggested  that  ureteric  peristalsis  played 
a contributory  part. 

I have  not  encountered  testicular  pain  in  cases  of  renal 
colic  due  to  an  aberrant  vessel,  and  I do  not  think  it  occurs  in 
cases  of  stationary  stone  in  the  kidney.  It  is  therefore  to  he 
regarded  as  a ureteric  and  not  a pelvic  or  renal  reference. 

Uterine  and  Tubal  Pain 

The  number  of  obstetric  and  gynaecological  cases  which 
comes  my  way  is  small,  and  I have  few  opportunities  of 
studying  their  pains.  As  with  dysmenorrhoea  and  parturi- 
tion, so  with  organic  disease  of  the  uterus,  back -ache  in  the 
sacral  area  is  a common  association.  Pain  down  the  front  of 
the  thigh  to  the  knee,  in  the  area  supplied  by  the  eleventh 
and  twelfth  dorsal  and  first  three  lumbar  segments,  is  an 
interesting  reference  accompanying  disease  of  the  pelvic 
organs  which  I have  encountered  once  or  twice,  and  which 
Marcus  [10]  has  particularly  associated  with  disease  of  the 
tubes,  citing  several  cases  of  salpingitis  and  ectopic  gesta- 
tion. Head  [11]  had  concluded  that  the  eleventh  and  twelfth 
dorsal  and  first  lumbar  were  the  segments  involved  in 
certain  uterine  cases.  Hilton  [7]  long  ago  suggested  that 
some  of  the  so-called  hysterical  pains  in  the  hip  and  knee 
might  depend  upon  reference  from  the  pelvic  organs,  and 
traced  the  path  of  the  impulses  via  the  sacral  and  lower 
lumbar  ganglia  to  the  sacral  nerves  and  obturator. 

Practical  Applications  of  tiie  Study  of  Pain 
< Thus  far  my  remarks  have  been  chiefly  concerned  with 
an  attempt  to  support  (in  the  case  of  each  viscus)  the 
hypotheses  set  forth  at  the  beginning  of  this  lecture.  Truism 
though  it  may  seem,  it  is  now  time  to  remind  ourselves  that 
a working  knowledge  of  the  causes  of  symptoms  is  of  great 
practical  importance,  perhaps  of  even  greater  importance 


cc  VISCERAL  PAIN  AND  REFERRED  PAIN 
to  the  physician  than  a knowledge  of  the  causes  of  disease. 
Of  nil  symptoms  pain  is  the  most  important.  In  the  earlier 
stages  of  our  education  a great  deal  of  time  was  and  still  is 
quite  properly  devoted  to  the  study  of  physical  signs — that 
is  to  say,  of  the  objective  evidences  of  structural  disease.  But 
symptoms,  being  invisible  and  impalpable,  are  too  often 
thought  to  be  poor  material  for  class  demonstration.  In 
practice  we  find  that  only  a small  proportion  of  our  cases 
have  physical  signs;  that  the  development  of  signs  is  nearly 
always  preceded  by  a period  of  symptoms ; and  that  again 
and  again  we  have  to  base  our  findings  on  the  anamnesis 
rather  than  on  the  physical  examination.  It  thus  becomes 
necessary  for  us  to  educate  ourselves  in  methods  of  analys- 
ing pains  as  accurately  as  possible,  in  collecting  information 
about  their  character,  situation,  and  attendant  phenomena, 
and  the  factors  by  which  they  are  intensified  or  relieved. 
We  have,  no  doubt,  been  taught  that  certain  pains  have 
certain  degrees  and  qualities;  that  the  severe  crises  like 
angina  and  renal  colic  ore  ‘agonizing’  and  ‘unbearable’; 
that  the  ‘spasmodic’  types  of  pain,  as  Heberden  [12J 
remarked,  arc  peculiarly  liable  to  come  on  in  the  middle  of 
the  night  or  the  early  hours  of  the  morning;  that  pain  in 
the  lateral  organs  does  not  as  a rule  cross  the  mid-line;  that 
intestinal  pains,  like  the  normal  peristaltic  movements  of 
the  intestine,  arc  rhythmical;  that  certain  pains  are  con- 
stantly relieved  by  certain  acts,  such  as  the  pain  of  duodenal 
ulcer  by  taking  food ; that  cardiovascular  pains  accompany 
effort;  that  gastric  pains  are  related  to  eating  or  fasting. 
Later  we  discover  for  ourselves  that  many  other  pains  and 
discomforts,  previously  but  dimly  understood,  may  have 
their  nature  revealed  by  careful  analysis,  although  the  most 
experienced  of  us  must  again  and  again  admit  defeat.  With 
hospital  patients,  and  with  private  patients  who  can  afford 
such  luxuries,  it  is  now  possible  to  subject  the  more  puzzling 
problems  to  fuller  investigation  and  so  to  correct  or  modify 
an  original  clinical  opinion.  The  possession  of  these  new 
facilities  should  never,  however,  excuse  us  from  careful 
clinical  inquiry.  The  ‘pathology  of  the  living’  studied  on 
the  operation  table  is  also  a valuable  corrective,  but  opera- 


VISCERAL  PAIN  AND  REFERRED  PAIN  67 

tion  should  rarely  be  resorted  to  for  purposes  of  diagnosis. 
One  of  the  most  important  things  in  studying  pain  is  to 
endeavour  to  see  the  patient  when  the  pain  is  actually 
present;  in  certain  circumstances,  in  order  to  assist  dia- 
gnosis, it  may  even  be  justifiable  to  take  steps  to  reproduce 
the  pain.  It  is  remarkable  how  rare  are  the  opportunities 
in  the  medical  wards  of  a hospital  and  in  consulting  practice 
for  seeing  the  patient  during  a bout  of  pain.  Even  in  general 
practice  the  patient  often  prefers,  or  is  compelled,  to  seek 
advice  between  attacks  unless  he  be  very  gravely  smitten. 

A technique  of  interrogation,  involving  ten  questions  and 
aimed  at  making  our  knowledge  of  an  individual  pain  more 
precise,  was  outlined  in  the  previous  lecture.  In  addition  to 
the  usual  routine  overhaul  an  examination  for  the  presence 
or  absence  of  referred  signs  should  always  be  made  in 
doubtful  cases,  and  this  is  particularly  important  in  dealing 
with  acute  or  chronic  abdominal  disorders.  The  difficulties 
with  which  we  have  to  contend  are  manifold.  They  in- 
clude the  limited  powers  of  observation  and  description 
possessed  by  many  patients;  the  ‘spread’  or  exaggeration 
of  certain  pains  in  nervous  or  debilitated  subjects;  the 
minimization  of  pain  by  others;  and  last,  but  by  no  means 
least,  the  shortness  of  life  in  comparison  with  the  length  of 
our  art.  In  general  practice  there  are  better  opportunities 
for  seeing  patients  repeatedly,  of  observing  minutely  varia- 
tions in  the  behaviour  of  their  symptoms,  and  of  assess- 
ing individual  physical  and  psychological  reactions  to  these 
symptoms.  Those  of  us  whose  work  is  of  a consulting  kind 
may,  on  the  other  hand,  have  better  opportunities  for  special 
investigations,  for  study  in  the  post-mortem  room,  and  for 
discussion  of  problems  with  colleagues.  For  all  of  us  the 
surgeon,  the  specialist,  and  the  pathologist  from  time  to 
time  will  furnish  proofs  which  have  long  been  waited  for, 
and  occasionally  a patient  with  unusual  powers  of  observa- 
tion may  greatly  illuminate  some  particular  point  of  doubt. 

Gnour  Study  of  Pain 

In  conclusion,  I should  like  to  suggest  that  there  is  no 
study  more  likely  to  furnish  interests  and  rewards  in  practice 


68  VISCERAL  PAIN  AND  REFERRED  PAIN 
than  a concerted  study  of  visceral  or  other  pains.  Results 
will  come  very  slowly,  but  this  need  not  discourage.  No 
apparatus  is  required,  no  laboratory  experience  is  necessary, 
and  yet  a valuable  piece  of  clinical  research  can  be  pursued  if 
four  or  more  men  in  one  town  will  set  to  work  to  keep  and 
pool  their  notes  of  all  cases  of  certain  types  of  pain.  Head- 
aches or  back-aches  may  be  studied  in  preference  to  stomach- 
aches or  heart -aches ; or  several  varieties  of  ache  may  be 
simultaneously  reviewed.  Such  inquiries  must  inevitably 
clear  the  mind  on  many  points  which  were  formerly  obscure, 
and  help  to  establish  facts  hitherto  imperfectly  established. 
And  finally,  even  though  time  or  inclination  for  special 
inquiry'  be  lacking,  each  one  of  us  can  bear  in  mind  a saying 
of  nilton’s  which  I am  never  tired  of  quoting:  ‘Every’  pain 
has  its  distinct  and  pregnant  signification,  if  we  will  but 
carefully  search  for  it.’ 

REFERENCES 

1.  Lennandeb,  K.  G.:  Centralbl.  f.  Chir.,  1010,  xxviii.  200,  and 
Joum.  Amer.  Med.  Assoc.,  1007,  xlix.  830. 

2.  Mackenzie,  J.:  Symptoms  and  their  Interpretation,  -4  th  cd., 
London, 1020. 

8.  Ross,  J.:  Brain,  1888,  x.  330. 

4.  IIuiist,  A.  F-:  Gouhlonian  Lect.  on  Sensibility  of  the  Alimentary 
Canal,  London,  1011. 

5.  Carlson,  A.  J. : Control  of  Hunger  in  Health  and  Disease,  Chicago, 
1010. 

0.  Waugh,  G.:  Lancet,  1025,  ii.  1054. 

7.  IIilton,  J.:  lectures  on  Best  and  Pain,  2nd  ed.,  London,  1877. 

8.  Head,  H.:  Brain,  1893,  xvi.  4. 

0.  op.  cit.,  70. 

10.  JIabcus,  M.:  Brit.  Mtd.  Joum.,  1D23,  i.  185. 

11.  Head,  H.:  op.  cit.,  89. 

12.  IlEBEnDEN,  IV. : Commentaries  on  the  History  and  Cure  of  Diseases, 
4th  ed.,  London,  1810. 


V 

THE  STUDY  OF  SYMPTOMS1 

The  clinical  appraisement  of  disease  in  man  is  customarily 
based  upon  inquiries  into  personal  and  family  history  and 
environment;  the  patient's  account,  both  voluntary  and 
elicited,  of  his  own  subjective  discomforts ; an  estimate  of 
his  physical  type  and  psychological  endowments;  and  a 
routine  examination  of  his  various  systems.  In  cases  of 
doubt  or  difficulty  we  may  further  employ  certain  instru- 
mental devices  such  as  the  electrocardiograph,  or  invoke 
the  aid  of  the  radiologist,  the  chemist,  or  the  bacteriologist. 
Where  none  can  be  neglected  it  would  be  difficult  indeed  to 
say  upon  which  department  of  such  an  inquiry  we  chiefly 
rely  for  our  opinions.  In  one  case  the  patient’s  ancestry  or 
his  own  previous  pathological  career  may  be  all-important, 
in  another  physiognomy,  or  the  physical  examination  may 
give  the  answer  to  our  question.  Often  a judicial  analysis 
of  all  available  information  is  necessary.  In  the  earlier  part 
of  our  clinical  training  it  is  usual  to  stress  the  importance  of 
physical  signs,  and  long  hours  are  properly  devoted  to 
practising  the  arts  of  palpation,  percussion,  and  ausculta- 
tion. Nevertheless  I am  persuaded  that  with  the  growth  of 
experience  pride  of  place  should  be  given  to  symptoms — 
that  is  to  say,  to  the  purely  subjective  phenomena  of  disease. 
Without  symptoms  patients  would  not  come  to  us  at  all. 
Symptoms  are  a part  of  morbid  physiology;  they  express 
disturbances  of  function.  As  a rule,  therefore,  they  precede 
the  development  of  signs  which  are  but  the  outward  morbid 
anatomy  of  the  living. 

In  the  first  days  of  practice  wre  are  often  baffled  by  the 
symptoms  which  our  patients  describe,  and  sometimes  dis- 
concerted when  we  find  so  little  of  an  objective  nature  to 
support  or  explain  them.  As  the  yearn  go  by,  however,  we 
begin  to  understand  and  to  be  grateful  for  symptoms.  Again 
and  again  we  find  ourselves  making  a reasonable  diagnosis 

1 Lancei,  3031,  i.  737. 


TO  THE  STUDY”  OF  SYMPTOMS 

while  we  sit  and  listen  to  the  patient’s  story  or  ply  him  with 
our  questions,  before  ever  his  clothes  have  been  removed 
or  a physical  sign  1ms  been  sought.  The  majority  of  patients 
have  indeed  little  to  show  in  the  way  of  physical  signs,  for 
these  depend  upon  advanced  structural  change.  But  even 
in  serious  forms  of  organic  disease  in  which,  sooner  or  later, 
definite  physical  abnormalities  become  apparent,  symptoms 
may  not  only  be  earlier  but  also  more  eloquent  than  signs. 
They  have,  therefore,  a particular  value  for  the  contributions 
which  they  make  to  early  diagnosis.  And  so,  on  the  score 
of  its  practical  utility  alone,  I hope  you  will  bear  with  my 
attempts  to  interest  you  in  a subject  which  might  at  first 
seem  to  be  on  elementary  part  of  the  daily  task  of  all 
students  of  medicine. 

There  is,  however,  anotheraspect  of  symptomatology,  and 
that  is  the  attraction  which  it  offers  as  a study  in  itself.  For 
many  of  us  the  philosophy  of  medicine,  which  runs  parallel 
with  the  art  of  medicine  pursued  for  humane  ends  and  with 
a view  to  ‘bread  and  butter’,  is  a perpetual  interest.  I am 
sure  we  should  endeavour  to  make  it  so,  for  the  joys  of 
practice  are  greatly  enhanced  if  we  can  also  gather  in  our 
work  some  of  the  crumbs  of  the  philosopher  or  the  natural 
historian. 

I shall  therefore  commend  to  you  the  study  of  symp- 
toms for  their  own  sake  as  well  as  for  the  sake  of  your 
patients  and  your  professional  reputations.  I do  so  the  more 
eagerly  because  I feel  that  the  subject  still  suffers  neglect 
in  our  generation  and  that  it  offers  a wide  field  for  future 
research. 


Methods  or  Study 

Two  important  papers  appeared  during  1931  in  the  British 
Medical  Journal,  one  by  Sir  ThomasLenis  en  titled  ‘Research 
in  Medicine:  Its  Position  and  its  Needs’,  and  the  other  by 
Mr.  Wilfred  Trotter  entitled  ‘Observation  and  Experiment 
and  their  use  in  the  Medical  Sciences’.  The  first  is  critical, 
stimulating,  even  provocative,  and  makes  an  appeal  on  be- 
half of  clinical  science  as  distinct  from  curative  medicine.  It 
suggests  that  the  experimental  study  of  disease  in  man,  as 


THE  STUDY  OP  SYMPTOMS  71 

supplementary  to  the  older  observational  method,  must 
shortly  come  into  its  own  and  appeals  for  the  appointment 
and  endowment  of  research  physicians  who  shall  be  relieved 
of  the  necessity  of  practice.  The  second  is  an  admirable 
philosophical  inquiry  into  the  relative  merits  and  achieve- 
ments of  the  observational  and  the  experimental  schools. 
In  the  biological  sciences  it  is  clear  that  observation  and 
experiment  must  ever  go  hand  in  hand.  The  great  clinical 
scientists  have  commonly  made  use  of  both.  It  is  certain 
that  experiment  will  play  a fuller  part  in  the  future,  but 
observation  must  continue  to  make  its  steady  contributions 
to  knowledge.  It  should  be  our  continual  concern  to  train 
better  observers  and  better  experimenters.  Now  it  is  obvious 
that  only  a minority  have  the  means,  the  aptitude,  or  the 
opportunity  essential  for  the  life  of  the  experimenter.  The 
majority  will  continue  to  enter  practice  in  one  form  or 
another,  and  every  one  of  these  must  do  his  best  to  become 
an  observer,  or  in  fact  a physician — a student  of  tf>vcrt$  or 
nature,  for  this  (as  Professor  Gairdner1  so  aptly  insisted  many 
years  ago)  was  the  original  interpretation  of  the  word.  The 
more  correctly  he  observes  and  the  more  carefully  he  sifts 
and  records  his  observations  the  better  practitioner  will 
he  be,  and  the  more  likely  is  it  that  he  will  render  useful 
service  to  clinical  science.  There  is  no  subject  that  he  will 
have  better  opportunities  of  studying  than  the  subject  of 
symptomatology,  for  he  will  live  in  the  midst  of  symptoms. 
It  will,  I think,  be  a very  long  time  before  symptoms  can  be 
studied  experimentally  on  any  considerable  scale.  Very  few 
of  them  can  be  accurately  reproduced.  The  majority  of 
them  as  they  occur  in  nature  are  transient.  We  have  no 
practical  method  at  present  of  measuring  or  photograph- 
ing subjective  phenomena.  They  express  the  behaviour 
of  diseased  or  disordered  tissues,  and,  like  the  behaviour  of 
plants  and  animals,  we  are  likely  to  learn  more  about  them 
by  constant  and  close  observation,  by  careful  recording,  and 
by  correlation  of  these  observations  with  objective  pheno- 
mena and  existing  physiological  knowledge  than  by  any 
other  process  of  study. 

1 The  Physician  as  Naturalist,  Glasgow,  1883. 


72  THE  STUDY  OF  SYMTTOMS 

If  %ve  pause  for  a moment  to  think  of  such  familiar  symp- 
toms as  pain  and  dyspnoea  we  realize  at  once  that,  while 
our  intimate  knowledge  is  slight,  we  can  already  classify 
them  into  several  varieties  of  pain  and  dyspnoea  and  that 
in  certain  instances  a particular  variety  has  a very  special 
significance.  When  it  has  a special  clinical  significance  it 
also  has  a special  physiological  significance,  and  the  nctual 
mechanism  of  the  pain  or  the  chemistry  of  the  breathless- 
ness in  such  case  has  commonly  been  proved.  In  time  it 
should  be  possible  to  sift  and  classify  and  analyse  nil  the 
subjective  phenomena  of  disease  in  the  same  way,  and  the 
meaning  of  nausea,  heartburn,  anorexia,  the  various  forms 
of  breathlessness,  vertigo,  the  various  headaches,  baek-aches, 
heart-aches,  and  stomach-aches,  thereferred  pains,  the  dysu- 
riasnnd  dysmenorrlioeas,  the  tinglings  and  numbnesses,  the 
fidgets  and  the  spots  in  front  of  the  eyes,  will  then  be  made 
more  clear  to  us.  It  can  scarcely  be  disputed  that  diagnosis, 
prognosis,  and  treatment  will  greatly  benefit  thereby. 

That  our  individual  studies  of  symptoms  may  prove  a 
pleasant  task  I shall  endeavour  to  show  out  of  my  own  small 
experience.  At  the  same  time  I shall  offer  more  detailed 
suggestions  for  the  conduct  of  the  observational  method  in 
this  field. 


Nature  and  Function  of  Symptoms 
Symptoms,  as  has  been  stated,  express  a disturbance  of 
function.  Although  they  are  often  caused  by  organic  disease 
they  do  not  express  the  disease  but  the  disturbance  of  func- 
tion which  the  organic  change  produces.  The  same  symp- 
toms may  thus  be  produced  by  functional  error  or  structural 
flaw.  While  not  specific  for  diseases,  symptoms  are,  never- 
theless, specific  for  functional  errors,  and  these  errors,  for 
the  most  part,  depend  upon  an  exaggeration,  a depression, 
or  an  inhibition  of  normal  reflex  phenomena.  The  dyspnoea 
of  great  effort  in  health  is  physiologically  similar  to  the 
dyspnoea  of  small  effort  in  heart  disease.  The  angina  of 
anxiety  or  tobacco  excess  or  anaemia  has  the  same  physio- 
logical basis  as  the  angina  of  coronary  sclerosis,  although 
none  of  its  gravity.  Gastric  and  intestinal  pain  as  severe 


THE  STUDY  OF  SYMPTOMS  78 

as  the  pain  of  gastric  ulcer  or  intestinal  obstruction  may 
occur  in  the  absence  of  gastric  or  intestinal  disease.  It 
is  by  the  character  and  behaviour  of  the  symptom  and  by 
its  associations  that  we  differentiate.  Giddiness  may  be  due 
to  cerebellar  disease,  to  slight  organic  changes  in  the  laby- 
rinth, or  to  transient  circulatory  effects.  Again  it  is  not  on 
the  symptom  itself  so  much  as  its  severity,  duration,  and 
associations  that  we  base  our  diagnosis. 

The  conception  of  symptoms  as  the  signals  of  functional 
disturbance  may  seem  a very  elementary  one,  but  it  is  none 
the  less  important.  It  is  as  such  rather  than  as  the  listed 
characteristics  of  diseases  that  we  should  wish  to  view  them. 
IVe  should  constantly  be  asking  ourselves  ‘ What  does  this 
symptom  mean?',  not  * What  is  it  a symptom  of  ? ' 

The  function  of  symptoms  is  presumably  protective. 
Dyspnoea  demands  general  rest  for  a local  and  general  ad- 
vantage. Pain  in  an  injured  limb  compels  local  rest  and  so 
permits  repair.  The  pain  of  angina  pectoris  demands  instant 
immobility  and  so  spares  the  heart  in  jeopardy  from  anox- 
aemia and  acute  muscle  failure.  The  pain  of  exaggerated 
hunger-tonus  in  duodenal  ulcer  calls  for  food-relief  with 
temporary  mechanical  and  chemical  rest  for  the  ulcer.  The 
pain  and  short,  shallow  respirations  of  pleurisy  and  pneumo- 
nia limit  the  expansion  of  the  chest  and  rest  the  inflamed 
pleura  and  lung.  ‘Pins  and  needles  ’ in  a cramped  limb  wake 
us  from  sleep  and  compel  us  to  restore  circulation  and  sensa- 
tion by  movement  and  friction.  Often,  we  must  confess, 
nature  seems  to  overdo  the  protective  stimulus,  for  pain 
may  be  out  of  all  proportion  to  the  size  and  gravity  of  the 
lesion.  Thus  the  pain  of  a minute  anal  ulcer  is  excessively 
severe  and,  although  the  spasm  of  the  sphincter  may  shut 
the  canal  against  the  passage  of  faeces,  it  is  in  itself  a cause 
of  added  pain  and  by  causing  constipation  may  even  aggra- 
vate the  trouble.  The  protective  significance  of  many  other 
symptoms  is  obscure,  but  for  the  most  part  they  are  symp- 
toms whose  nature  remains  at  present  undetermined.  In  a 
more  remote  and  less  biological  sense  symptoms  in  man  are 
protective  in  that  they  compel  their  victim  to  seek  the 
advice  and  aid  of  others. 


74  TIIE  STUDY  OF  SYMPTOMS 

The  remote  physical  symptoms  of  anxiety,  hypochondria, 
and  other  psychic  disturbances  are  of  central  origin  or  to  he 
referred  to  the  emotional  plane.  They  may  be  due  to  a loss 
of  balance  between  vagal  and  sympathetic  activity,  or  they 
may  be  called  into  action  ns  a mask  for  truth  or  as  a plea  for 
sympathy.  It  is  also  an  early  lesson  of  practice  that  the 
degree  of  symptoms  primarily  due  to  physical  causes  may 
be  increased  by  anaemia,  general  debility,  temperamental 
factors,  or  psychic  states.  Such  modifications  provide  one  of 
the  most  considerable  difficulties  encountered  in  the  assess- 
ment of  the  subjective  phenomena  of  disease. 

Tna.EE  Symptoms 

1 propose  to  review  some  elementary'  observations  on 
three  very  diverse  symptoms,  all  likely  to  be  encountered  in 
general  practice  or  medical  consulting  practice,  all  capable 
of  expressing  organic  change  or  functional  disorder,  but  nil 
— properly  assessed — of  the  greatest  help  in  distinguishing 
organic  from  functional  disease. 

The  first  symptom  is  a type  of  abdominal  pain  originating 
in  the  colon.  Sometimes  of  considerable  severity,  it  is  one 
for  which  operations  are  frequently  but  fruitlessly  per- 
formed. The  suggested  method  of  analysis  of  this  pain  may' 
stand  as  an  example  for  the  analysis  of  any  other  viscera] 
pain,  and  as  one  plan  of  attack  in  the  observational  study 
of  subjective  phenomena. 

The  second  symptom  is  nausea.  It  is  one  which  may  be 
evoked  in  health  and  which  occurs  in  a variety-  of  physical 
disorders.  The  method  of  considering  the  common  factor 
or  factors  in  the  widely  varied  conditions  in  which  it  occurs 
is  another  obvious  method  of  approach  to  an  individual 
symptom. 

The  third  symptom  is  one  of  the  strangest  but  apparently' 
one  of  the  most  real  and  vivid  of  ah  subjective  phenomena. 

It  is  the  sense  of  dying,  the  feeling  of  impending  dissolution , 
or  angor  animi,  which  in  the  literature  is  usually  associated 
with  angina  pectoris  but  which  also  occurs  in  several  other 
conditions,  as  I shall  show,  and  most  frequently’  in  the 
absence  of  serious  structural  disease.  This  symptom  being. 


THE  STUDY  OF  SYMPTOMS  75 

like  nausea,  less  precise  and  definable  than  pain,  requires 
other  measures  of  analysis. 

Colonic  Pain 

The  particular  type  of  abdominal  pain  on  which  these 
observations  are  based  occurs  as  a rule  in  the  absence  of 
any  demonstrable  organic  change  and  is  the  expression 
of  tonic  over-activity  or  sustained  spasticity  in  the  colonic 
musculature.  It  is  frequently  troublesome  and  persis- 
tent, sometimes  very  severe,  and  quite  commonly  leads 
to  nppendicectomy  or  exploratory  operations.  Here  is  an 
account  of  a case: 

A man,  aged  30,  of  spare  habit  and  nervous  temperament,  first 
began  to  experience  abdominal  pains  at  the  time  of  bis  final  examina- 
tions in  medicine.  After  a period  of  freedom  they  recurred  when  he 
sat  for  Ids  final  Fellowship.  They  were  referred  to  the  right  side  of 
the  abdomen.  Later  he  experienced  them  in  the  upper  abdomen  and 
occasionally  lie  had  pain  in  both  iliac  fossa.  In  the  past  he  had 
suffered  from  astlima  and  migraine.  When  he  first  consulted  me  he 
had  been  examined  with  X-rays  on  no  less  than  six  occasions,  and 
had  been  diagnosed  as  having  both  a hypertonic  and  a hypotonic 
stomnch,  and  ns  a case  of 'nerves’.  Fatigue  and  worry  were  the  chief 
aggravating  factors.  On  one  occasion  he  thought  be  bad  appendicitis, 
but  then  discovered  that  what  he  took  for  rigidity  was  a hardened 
caecum  or  ascending  colon.  I found  a cord-like  descending  colon, 
and  on  another  occasion  an  easily  palpable  and  contracted  ascending 
colon.  With  reassurance  and  modifications  in  his  mode  of  life  his 
health  improved  greatly.  In  bis  attacks  he  found  that  belladonna 
gave  him  great  relief. 

The  condition  has  been  variously  described  as  spastic 
colon,  spasmodic  constipation,  and  tonic  hardening  of  the 
colon.  It  is  a visceral  neurosis  akin  to  asthma.  Its  aetio- 
logical  characters  arc  discussed  more  fully  in  Lecture  XII ; 
and  its  morbid  physiology  in  Lecture  XI.  Anxious  to  investi- 
gate the  nature  of  the  disorder  and  the  cause  of  the  pain,  I 
analysed  my  notes  of  SO  cases  and  applied  to  the  pain  itself 
certain  tests  or  queries  which  have  been  helpful  to  me  in  the 
study  of  other  pains.  These  tests  or  queries,  already  listed  in 
Lecture  III,  are  in  the  form  of  ten  questions  relating  to:  (1) 
the  character  of  the  pain;  (2)  its  degree  or  severity;  (3) 
its  situation ; (4)  its  localization  or  extent  of  diffusion ; (6)  its 


76  THE  STUDY  OF  SYMPTOMS 

paths  of  reference ; (C)  its  duration ; (7)  its  frequency ; (8)  its 
special  times  of  occurrence ; and  (9)  and  (10)  its  aggravating 
and  relieving  factors.  These  arc  finally  correlated  with 
associated  symptoms  and  objective  phenomena. 

The  purpose  of  these  questions  is  simply  to  make  our 
knowledge  of  the  pain  more  precise.  Too  often  we  are  con- 
tent with  the  patient’s  statements  that  he  has  a ‘pain  in  his 
belly’.  As  anatomists,  physiologists,  and  psychologists  wc 
should  desire  to  know  much  more  than  that,  and  even  if  we 
are  not  dealing  with  measurable  things  wc  should,  when- 
ever time  and  opportunity  permit,  evolve  methods  of  im- 
proving our  standards  of  clinical  accuracy. 

The  answers  to  these  questions  in  the  case  of  spastic  colon 
are  ns  follows: 

(1)  The  character  of  the  pain  is  a 'dull,  steady  ache’,  sometimes 
gnawing  and  never  ‘griping’  as  in  the  peristaltic  pain  of  purgation 
or  obstruction. 

(2}  Usually  * bearable  ’ it  is  occasionally  so  severe  as  to  suggest  one 
of  the  major  ‘colics*. 

(8)  Its  situation  is  in  the  course  of  the  ascending,  the  descending, 
or  transverse  portions  of  the  colon,  in  this  order  of  frequency.  It 
may  occur  in  one  or  more  of  these  situations  simultaneously.  There 
may  also  be  rectal  pain. 

(4)  and  (5)  The  localization  corresponds  accurately  with  the  true 
surface  marking  or  radioiogically  observed  course  of  the  colon.  Some- 
times it  is  more  diffuse.  Referred  pain  and  tenderness  in  the  somatic 
planes  are  rare. 

(6)  and  (7)  The  duration  of  the  pain  may  be  for  an  hour,  hours,  or 
even  days.  Its  frequency  is  very  variable  and  depends  largely  on 
personal  and  environmental  factors. 

(8)  A special  time  of  occurrence  is  2 or  3 bouts  after  food,  and  of 
non-occurrence  during  the  night  when,  with  warmth  and  physical 
nnd  mental  relaxation,  the  pain  usually  departs. 

(0)  Aggravating  factors  include  cold,  fatigue,  worry,  constipation, 
purgatives,  jolting,  exercise,  and  tobacco. 

(10)  Relieving  factors  include  warmth,  holidays,  belladonna,  and 
large  warm  enemata. 

Associated  symptoms  include  constipation  frequently  and 
diarrhoea  less  frequently;  dysmenorrhoea;  urinary  fre- 
quency ; and  ‘dead  fingers  ’ in  cold  weather.  The  chief  objec- 
tive finding  is  a readily  palpable  and  firmly  contracted  colon 
due  to  tonic  rigidity,  shortening,  and  straightening  of  the 


THE  STUDY  OF  SYMPTOMS  77 

affected  portion.  The  sigmoidoscope  may  show  a sustained 
spasm  synchronous  with  pain.  An  X-ray  examination  may 
reveal  thread-like  narrowing  of  the  bowel  lumen,  straighten- 
ing of  the  affected  loop,  and  disappearance  of  natural  haus- 
trations. 

From  these  and  other  observations  it  seems  only  reason- 
able to  conclude  that  the  pain  itself  is  due  to  a sustained 
tonic  contraction  of  the  bowel,  and  that  this  depends  upon 
an  inherent  irritability  occurring  in  association  with  certain 
physical  and  temperamental  types. 

What  are  the  practical  and  the  philosophical  advantages 
of  such  an  inquiry?  In  practice  it  enables  us  with  greater 
confidence  and  a diminishing  margin  of  error  to  differentiate 
an  important  visceral  neurosis  from  appendicular  disease, 
duodenal  ulcer,  diverticulitis,  carcinoma  coli,  renal  and 
biliary  colic,  ovarian  and  tubal  disease,  and  hypochondria. 
All  of  these  at  times  have  been  alternative  diagnoses  in  the 
minds  of  myself  or  of  colleagues  who  have  referred  cases 
of  this  kind  to  me. 

The  philosophical  value  comes  from  the  application  of  a 
definite  method  to  a simple  clinical  inquiry  and  from  the 
small  increments  of  knowledge  gained  thereby.  To  the 
physiologist  or  the  physicist  the  procedure  may  seem  clumsy 
and  lacking  in  anything  savouring  of  exactitude,  dealing  as 
it  does  with  processes  which  cannot  be  measured.  Never- 
theless their  precise  experimental  methods  would  find  no 
application  at  the  present  time  in  the  solution  of  such  a 
problem.  To  the  field  naturalist — and  the  physician  is  the 
field  naturalist  of  medicine — the  procedure  might  appear 
as  a reasonable  and  appropriate  attempt  to  improve  the 
accuracy  of  the  observational  method. 

Nausea 

With  a symptom  such  as  nausea  we  are  in  greater  diffi- 
culty for,  although  we  understand  quite  clearly  what  we 
mean  by  nausea,  we  can  scarcely  describe  it  in  the  way  that 
we  can  describe  a pain.  Even  its  localization  is  a difficult 
matter,  and  at  present  we  must  accept  that  it  is  felt  in  the 
pharynx  and  the  epigastrium,  sometimes  more  in  one  place 


78  THE  STUDY  OF  SYMPTOMS 

than  the  other,  sometimes  in  both  together-  General  sensa- 
tions of  malaise  and  faintness  commonly  accompany  it-  The 
symptom  can  be  engendered  in  various  wavs  in  healthy 
people.  Some  are  more  sensitive  than  others,  and  women 
are  more  readily  afflicted  than  men.  A revolting  sight  or 
smell  or  even  the  thought  or  recollection  of  something  un- 
pleasant may  induce  it,  and  here  it  provides  a good  example 
of  the  conditioned  reflex.  The  ingestion  of  greasy  or  fatty 
dishes,  of  paraffin  or  castor  oil,  or  the  smell  of  frying — all 
these  particularly  in  hot  weather,  when  the  appetite  sense 
is  dulled — are  familiar  provocatives  of  nausea.  Of  foodstuffs 
it  is  particularly  noteworthy  that  fats  and  oils  arc  the  most 
culpable,  crisp  and  savoury  foods  the  least.  It  appears  more 
easily  after  repletion.  The  things  which  engender  appetite 
combat  it;  those  which  destroy  appetite  encourage  it.  Ano- 
rexia and  nausea  arc  very  close  allies.  Now  certain  emotions, 
oils  and  fats — as  can  be  shown  experimentally — all  have 
the  property  of  inhibiting  gastric  tonus,  peristalsis,  and 
secretion.  An  oily  or  cream}'  test-meal,  as  I have  proved  in 
my  own  person  [1],  takes  twice  as  long  to  leave  the  stomach 
as  a gruel  test-meal  and  evokes  a much  slighter  add  re- 
sponse. Similar  effects  were  produced  by  the  suggestion  of 
nausea  under  hypnosis  by  Bennett  and  Venables  [2].  Appe- 
tite and  hunger  and  well-being  on  the  other  hand  are  associ- 
ated with  activated  tonus,  peristalsis,  and  secretory  activity. 
In  practice  we  meet  with  nausea  in  chronic  gastritis,  in 
which  the  normal  responses  of  the  stomach  arc  inhibited 
by  the  thick  layers  of  mucus  which  coat  its  membranes ; in 
jaundice  and  cholecystitis,  conditions  in  which  fatty  foods 
are  badly  tolerated ; and  in  anaemic  states,  in  which  appetite 
is  diminished  when  the  stomach,  like  the  heart,  sharing  the 
general  anaemia,  sutlers  loss  of  its  usual  functional  efficiency. 
In  the  presence  of  acute  peripheral  pain  and  emotional 
states,  in  faintness  and  vertigo,  the  stomach  expresses  with 
nausea  the  general  consequences  illustrated  in  the  case  of 
the  vasomotor  system  by  pallor  and  shock-like  phenomena. 
In  each  case  the  tone  of  plain  muscle  is  Inhibited. 

Nausea  is  absent  conversely  in  those  painful  gastric  dis- 
turbances like  duodenal  ulcer,  in  which  tonic  and  peristaltic 


THE  STUDY  OF  SYMPTOMS  70 

activity  are  exaggerated.  One  of  the  most  interesting  demon- 
strations of  the  behaviour  of  the  stomach  during  nausea  is 
given  by  screening  after  a barium  meal  during  an  attack  of 
migraine.  The  stomach  is  then  seen  to  be  inert,  the  barium 
lying  as  in  a bag,  with  little  or  no  peristalsis  and  prolonged 
delay  in  emptying.  Barclay  [8]  has  observed  a drop  of  3 
inches  in  the  lower  border  of  the  stomach  just  before  faint* 
ing  occurred  and  has  recorded  the  same  event  in  the  case  of 
a patient  who  was  given  nauseous  substances  to  smell. 

From  parallel  clinical,  physiological,  pathological,  and 
radiological  observations  such  as  these  we  conclude  that  the 
gastric,  and  that  is  perhaps  the  major,  part  of  nausea  is 
associated  with  a depression  or  inhibition  of  the  normal 
tonic  and  peristaltic  functions  of  the  stomach.  When  con- 
fronted with  nausea  in  practice  it  is  particularly  important 
to  discover  whether  it  occurs  in  concert  with  headache  as  in 
migraine  and  some  cases  of  astigmatism,  or  with  giddiness 
as  in  labyrinthine  disease;  whether  it  has  a morning  inci- 
dence as  in  pregnancy  and  gastritis;  whether  anaemia  or 
anxiety  be  evident;  or  whether  it  comes  in  ‘waves’  and  is 
associated  with  scapular  pain  and  right  subcostal  pain  as 
in  cholecystitis.  Its  time  relationships  and  symptomatic 
associations  rather  than  the  symptom  itself  are  the  helpful 
points  in  diagnosis.  If  we  except  the  hypnotic  experiment 
and  Barclay’s  experiment  with  smells  our  information  con- 
cerning nausea  may  be  said  to  have  been  mainly  deduced 
from  physiological  information  and  clinical  observation. 
It  is  difficult  to  suggest  at  present  how  it  might  be  more 
usefully  studied  experimentally.1 

The  Sense  of  Dying 

We  come  lastly  to  that  strange  symptom  usually  referred 
to  ns  the  sense  of  dying,  the  feeling  of  impending  dissolu- 
tion, or  angor  animi.  Until  this  has  been  experienced  it 
would  seem  that  we  can  have  no  conception  of  its  character. 
With  rare  exceptions  it  is  not  present  even  on  the  threshold 

1 E.  1*.  Toulton  and  W.  W.  Puyne  (Joum.  of  rhytiology,  1023,  her. 
157)  by  personal  experiment*  liave  demonstrated  oesophageal  relaxation 
In  association  with  nausea. 


80  TIIE  STUDY  OF  SYMPTOMS 

of  death.  It  has  no  kinship  with  pain  or  other  familiar 
bodily  discomfort.  It  differs  from  nil  ordinary  forms  of 
faintness.  And  yet  it  is  more  real  and  arresting  and  distress- 
ing to  its  victims  than  any  of  these.  It  is  not  mere  anxiety 
or  panic  and,  although  it  necessarily  engenders  apprehen- 
sion, it  is  quite  wrong  to  describe  it  as  the  fear  of  impending 
dissolution.  I have  known  two  courageous  young  men, 
dangerously  occupied,  who  suffered  from  it.  Clifford  Allbutt 
insisted  that  it  should  be  considered  as  *nn  organic  sensa- 
tion’ [4],  and  so,  for  many  reasons,  I believe  it  to  be.  Accord- 
ing to  my  own  notes  it  occurs  in  some  20  per  cent,  of  cases 
of  angina  pectoris  and  distinctly  less  frequently  in  the  status 
onginosus  of  coronary  thrombosis  than  in  the  angina  of 
effort.  I have  also  recorded  it  in  angina  cruris — so-called 
intermittent  claudication,  and  in  a case  of  Raynaud’s 
disease,  in  each  of  which  it  was  synchronous  with  the  vas- 
cular manifestations  [5],  It  occurs  in  10  per  cent,  of  cases  of 
labyrinthine  vertigo.  It  may  accompany  anaphylactic  shock. 
Sir  Arthur  Hurst  told  me  that  he  had  noted  it  after  injec- 
tions of  adrenalin.  I find  that  it  is  present  in  no  less  than  CO 
per  cent,  of  my  eases  of  that  peculiar  syndrome  described  by 
Gowers  as  the  vaso-vagal  attack,  and  by  German  authors  as 
angina  vasomotoria.  In  most  of  the  remaining  40  per  cent, 
of  cases  kindred  sensations  as  of  ‘fading  away’  or  ‘going 
under  an  anaesthetic’  arc  mentioned.  Finally  it  may  occur 
in  organic  central  nervous  disease  involving  a precise  and 
particular  localization  which  seems  to  lend  confirmation  to 
the  hypothesis  I have  advanced  [5]  in  regard  to  the  genesis 
of  the  symptom. 

As  my  best  opportunities  of  observing  angor  animi  have 
been  in  cases  of  the  vaso-vagal  syndromel  shall  here  describe 
two  characteristic  cases: 

Case  3.  A woman  of  02,  who  had  previously  been  under  my  care 
for  general  ill  health  and  cholecystitis,  became  the  victim  of  severe 
emotional  stress  and  developed  attacks  of  retrosternal  pain  with  a 
sense  of  constriction  in  the  chest  and  tingling  in  the  left  arm.  In  the 
attacks  her  husband  described  her  as  of  ‘the  colour  of  a piece  of 
marble’.  Gradually  the  character  of  the  attacks  changed.  The  main 
symptom  was  now  a sense  of  dying,  out  of  the  belief  in  which  she 
could  in  no  way  be  persuaded.  With  it  she  felt  an  extreme  sense  of 


THE  STUDY  OF  SYMPTOMS  81 

constriction  of  the  chest  and  experienced  a curious  feeling  between 
her  left  clavicle  and  her  neck  as  though  the  head  were  being  drawn 
down  on  that  side.  She  also  had  tingling  in  the  fingers.  The  attacks 
would  last  from  half  an  hour  to  one  hour,  were  not  induced  by  effort, 
and  she  remained  with  a feeling  of  profound  prostration  for  several 
days  afterwards.  In  the  attacks  she  was  pale  and  cold.  Her  pulse- 
rate,  normally  70,  fell  sometimes  as  low  as  82  to  the  minute,  and  I 
myself  counted  it  at  44  at  the  end  of  an  attack.  Brandy  gave  some 
relief;  tabelJae  trinit rini  little  or  none.  Her  blood-pressure  varied 
remarkably  from  time  to  time  between  130-80  and  180-90.  In  one 
very  bad  attack  she  lost  consciousness  and  the  pulse-rate  fell  to  19 
to  the  minute.  The  respirations  were  rapid  and  shallow.  Her  hus- 
band, a medical  man,  was  convinced  that  she  was  dying.  She  was 
made  to  inliale  amyl  nitrite  when  the  pulse  quickly  rose  to  52  and 
some  colour  returned.  There  was  no  clinical,  electrocardiographic,  or 
radiological  evidence  of  arteriosclerosis  or  heart  disease.  Eventually 
removal  from  the  causes  of  her  emotional  stress  cured  her  of  all  the 
major  attacks,  although  she  still  had  an  occasional  return  of  prae- 
cordial  discomfort  and  the  strange  feelings  above  the  clavicle. 

Case  2.  A man  of  57  had  his  first  and  only  attack  on  board  ship 
during  a rough  sea  when  for  the  first  time  in  Ids  life  he  suffered  sea- 
sickness. In  the  lavatory  he  suddenly  felt  dreadfully  ill,  became  stiff 
and  rigid,  was  unable  to  speak,  move,  or  draw  in  a deep  breath,  and 
was  convinced  that  he  was  dying.  In  this  condition  he  was  found  by 
chance  and  carried  to  the  deck  by  a sailor.  There,  when  he  at  last  got 
Ids  breath,  he  felt  as  if  he  had  received  a sudden  blow  at  the  back  of 
Ids  neck. 

From  these  cases  and  many  others  we  learn  that  the  vaso- 
vagal syndrome  may  include  the  following  symptoms:  First 
and  foremost  the  sense  of  dying,  and  after  this  prostration, 
coldness,  immobility,  constricted  breathing,  and  tingling  or 
a leaden  feeling  in  the  arms,  and  often  pain  or  discomfort  of 
anginal  distribution.  Objectively  the  patient  is  pale,  the 
pulse  is  very  slow  or  quickened,  the  respirations  are  shallow 
and  rapid,  and,  probably  as  a result  of  this,  minor  tetany 
may  be  present.  There  are  thus  the  same  sense  of  constric- 
tion and  immobility  which  accompany  angina  pectoris, 
together  with  disturbances  of  cardiac  sensation.  There  are 
the  same  pallor  and  vasomotor  disturbance  which  accom- 
pany shock,  fainting,  and  vertigo.  Prostration  follows  such 
as  is  seen  in  migrainous  attacks.  Unconsciousness  occurs 
occasionally  to  remind  us  or  epilepsy  and  fainting.  There 
are  remarkable  variations  in  pulse-rate  and  blood-pressure. 

o 


82  THE  STUDY  OF  SYMPTOMS 

All  these  events  point  to  some  profound  nervous  storm, 
and  some  of  the  phenomena,  such  as  the  bradycardia,  inevit- 
ably suggest  a vagal  influence.  There  are  ample  reasons 
why  Gowers  should  have  included  the  syndrome  in  his 
classical  monograph  on  The  Borderland  of  Epilepsy.  A Case 
has  recently  been  described  in  whichavaso- vagal  attack  was 
always  followed  later  in  the  day  by  a true  epileptic  seizure  [G]. 

Vaso-vaga!  attacks,  in  my  experience,  almost  invariably 
occur  in  persons  who  are  afflicted  simultaneously  by  chronic 
or  recurring  mental  distress  and  by  some  general  cause  of 
physical  ill  health,  such  as  anaemia,  digestive  disorder,  the 
menopause,  or  a chronic  infection.  In  one  case  the  attacks 
were  repeatedly  precipitated  by  the  uncomfortable  visceral 
stimulus  of  colonic  irrigation,  and  I have  notes  of  other 
cases  in  which  disturbed  function  in  one  or  other  of  the 
hollow  viscera  was  associated  with  angor  animi.  Something 
similar  in  respect  of  the  associated  malaise  and  shock  has 
also  been  induced  in  healthy  men  by  arterial  puncture  [7]. 
In  angina  pectoris  the  angor  may  be  synchronous  with  the 
pain  and  the  sudden  arrest  of  movement.  This  powerful 
triple  reflex  is  Nature’s  ’pistol  to  the  head’.  ‘Another  step 
and  you  are  a dead  man’  would  seem  to  be  its  purport.  It 
would  seem  that  an  emotional,  a visceral,  or  a vascular 
stimulus  may  be  the ' trigger’  for  angor  animi,  buttbatin  the 
absence  of  general  ill  health  and  nervous  instability  of  con- 
stitutional origin,  or  brought  about  by  anxiety,  it  is  unusual 
for  the  full  vaso-vagnl  attack  to  follow. 

Viewing  the  vaso-vagnl  syndrome  as  a variety  of  nervous 
storm,  akin  to  epilepsy  and  migraine,  and  having  particular 
regard  for  the  vagal  phenomena  and  the  sinister  leading 
symptom,  it  has  seemed  not  unnatural  to  suggest  that  the 
medullary  level,  where  the  centres  of  life  itself  reside,  might 
be  involved  in  this  storm.  It  is  at  this  point  that  we  must 
begin  to  look  for  proofs  of  the  hypothesis.  My  colleague  Sir 
Charles  Symonds  has  told  me  of  two  interesting  cases  in 
which  he  has  encountered  the  sense  of  dying  in  association 
with  organic  central  nervous  disease.  One  case  was  that  of 
& child  with  signs  of  a tumour  involving  the  medulla  oblon- 
gata. The  other  was  that  of  a man  with  central  nervous 


THE  STUDY  OF  SYMPTOMS  83 

syphilis  who  was  found  at  necropsy  to  have  miliary  gum- 
mata  in  the  same  situation.  I have  under  my  care  at  the 
moment  a middle-aged  man  with  tabes  dorsalis  and  severe 
vaso-vagal  seizures. 

May  we  not  venture  to  claim  that  our  symptom,  although 
still  very  imperfectly  understood,  has  been  tracked  to  its 
point  of  nervous  origin?  I believe  we  may. 

The  practical  outcome  of  these  considerations,  apart 
from  their  contributions  to  diagnosis,  is  that,  excepting  in 
angina  pectoris  of  organic  origin  or  such  a rare  mischance 
as  disease  of  the  medulla  itself,  the  alarming  sense  of  dying 
has  no  grave  prognostic  significance.  In  vertigo  and  vaso- 
vagal attacks  we  may  give  the  fullest  reassurance  and  so 
find  ourselves  in  a much  better  position  to  handle  the  situa- 
tion wisely  than  we  should  do  if  perplexed  by  the  distressing 
character  of  the  patient’s  complaint  and  the  disquieting 
objective  manifestations  of  the  attacks. 

Conclusion 

Let  us  briefly  review  the  methods  employed  in  the  in- 
vestigation of  these  three  symptoms,  for  they  may  perhaps 
serve  as  a guide  to  the  investigation  of  other  subjective 
phenomena. 

In  the  case  of  the  particular  pain  of  spastic  colon  the 
method  was  firstly  to  define  the  symptom  itself  by  estimat- 
ing its  degree  and  discovering  the  special  qualities  peculiar 
to  it,  and  then  to  review  carefully  its  associations  in  the 
shape  of  other  symptoms,  physique,  temperament,  and 
objective  findings. 

In  the  case  of  nausea,  a familiar  symptom  but  one  lacking 
the  precision  of  pain,  the  method  was  to  consider  common 
experience,  the  physiological  end  pathological  provocatives 
of  the  symptom,  the  various  disorders  in  which  it  is  promi- 
nent, and  the  factors  common  to  these.  Finally  we  obtained 
the  help  of  certain  objective  studies  of  the  stomach  by  X- 
rays  during  bouts  of  natural  and  induced  nausea. 

In  the  case  of  angor  animi,  or  the  sense  of  dying  (a  symp- 
tom which  is  quite  beyond  imagination  and  common  experi- 
ence, but  one  which  is  felt  intensely  and  described  with  an 


84  THE  STUDY  OF  SYMPTOMS 

emphasis  or  horror  giving  it  a reality  as  impressive  as 
the  reality  of  pain),  the  method  was  again  to  consider  the 
known  conditions  in  which  it  occurs,  to  record  and  correlate 
associated  phenomena  in  each  of  these,  to  advance  the 
hypothesis  that  the  symptom  could  best  be  explained  as 
being  due  to  some  disturbance  involving  the  neighbourhood 
of  the  vagal  nuclei,  the  realm  that  governs  the  functions  of 
life  itself,  and  then  finally  to  discover  that  organic  disease  in 
that  confined  region  is  in  fact  capable  of  reproducing  the 
symptom. 

The  methods,  in  brief,  were  those  of  observation,  record, 
and  analysis.  The  conclusions  to  which  they  lead  us  are  as 
yet  provisional  and  incomplete.  It  is  not  to  be  expected 
that  the  results  of  such  methods  will  ever  have  the  finality' 
of  successful  experiment,  but  wc  are  entitled  to  urge  that 
they  arc  scientific  and  serviceable.  They'  are  scientific  be- 
cause they  constitute  a systematic  inquiry  after  truth.  They 
are  serviceable  because  they  provide  a useful  exercise  for  the 
mind ; because  they  carry'  us  beyond  ignorance  and  furnish 
us  with  reasonable  hypotheses ; and,  most  of  all,  because 
they  improve  diagnosis,  prognosis,  and  treatment. 

REFERENCES 

1.  Ryle,  J.  A. : Gastric  Function  in  Health  and  Disease,  London,  1020. 

2.  Bennett,  T.  I.,  and  Venables,  J.  F.:  Brit.  Med.  Joum.,  1020,  ii. 

002. 

а.  Barclay,  A.  E.:  The  Lancet,  1022,  ii.  201. 

4.  Allbutt,  Clifford:  Diseases  of  the  wineries  including  Angina 

Pectoris,  London,  1015. 

5.  Ryle,  J.  A.:  Guy's  IIosp.  Rep.,  1028,  lxxviii.  571. 

б.  JJUJR.:  Guy's  IIosp.  Gaz.,  1030,  xliv.  110. 

7.  Bazett,  H.  C.,  and  McGlone,  B.:  Drain,  1028,  li.  18. 


VI 


THE  NATURE  AND  RELIEF  OF  SOME  COMMON 
GASTRIC  SYMPTOMS1 

The  science  of  symptomatology,  whatever  appeal  it  may 
make  to  our  philosophy,  is  essentially  a practical  science. 
Its  concern  is  with  common  things,  for  symptoms  are  always 
and  everywhere  available.  If  we  analyse  our  diagnostic 
achievements  we  find,  with  the  passage  of  time,  that  they 
depend  more  often  upon  a proper  appreciation  of  subjective 
symptoms  than  upon  any  special  skill  or  training  in  the 
methods  of  physical  examination.  To  accurate  history- 
taking  and  the  study  of  personality  full  credit  must  be 
given,  and  the  routine  overhaul  must  never  suffer  neglect, 
but  a detailed  interrogation  in  respect  of  the  patient’s  own 
sensations  is  the  physician’s  surest  tool. 

In  practice  only  a small  proportion  of  our  patients  are 
found  to  present  frank  physical  signs,  and  when  they  do  so 
their  disease  is  active  or  advanced.  But  no  patient,  unless  it 
be  for  purposes  of  life  insurance  or  a health  certificate, 
comes  to  us  without  a symptom.  It  is  true  that  we  all  learn 
to  associate  certain  symptoms  or  groups  of  symptoms  with 
certain  diseases,  disorders,  histories,  and  temperaments,  and 
so  by  degrees  make  better  use  of  them.  But  we  should  not 
rest  content  with  this  knowledge;  we  should  seek  to  dis- 
cover the  fuller  physiological  significance  of  each  symptom, 
for  then  its  value  is  doubled. 

If  physical  signs  may  be  called  the  morbid  anatomy  of 
bedside  medicine,  symptoms  are  its  morbid  physiology,  and 
they  usually  precede  the  development  of  signs.  This  is  well 
shown  by  any  familiar  symptom,  such  as  angina  pectoris, 
in  the  presence  of  which  we  are  often  entitled  to  surmise  the 
presence  of  coronary  arteriosclerosis  long  before  the  stetho- 
scope or  the  electrocardiograph  can  demonstrate  organic 
change.  Each  symptom  expresses  a perturbation  of  some 
normal  function,  an  exaggeration  or  a depression  of  a 

1 Cuyi  Ilotp.  Gazette,  1031,  xlvlll.  463, 


80  THE  NATURE  AND  RELIEF  OF 

healthy  vital  reflex.  The  dyspnoea  of  exertion  in  health  is 
physiologically  allied  to  the  dyspnoea  of  heart  disease  at 
rest.  Many  of  the  symptoms  of  disease,  such  as  dyspnoea, 
dizziness,  and  nausea,  can  be  reproduced  by  suitable  over- 
actions  or  inhibitions  artificially  induced  in  healthy  subjects. 

In  no  group  of  diseases  do  we  have  to  rely  more  upon 
symptoms  than  those  collected  under  the  general  heading 
of  the  dyspepsias.  The  descriptions  of  their  feelings  which 
patients  furnish  may  be  vague  or  confusing  at  times,  but 
this  is  partly  our  own  fault,  because  we  are  not  sufficiently 
at  pains  to  develop  a proper  technique  of  interrogation. 

The  majority  of  the  dyspepsias  are  due  to  errors  of  gastric 
or  oesophageal  function  occurring  independently  of  organic 
disease,  but  even  in  the  presence  of  organic  disease  we  arc 
commonly,  from  the  nature  and  small  size  of  the  lesion  and 
the  inaccessibility  of  the  viscera,  deprived  of  the  advantages 
of  objective  evidence. 

Before  directing  attention  to  the  six  symptoms  which  it 
is  my  purpose  to  review,  let  me  remind  you  briefly  of  what 
is  known  of  the  normal  sensibility  of  the  stomach.  Appetite, 
hunger,  satiety,  and  repletion  are  all  normal  sensations,  and 
in  part,  at  least,  appreciated  by  the  stomach  itself.  To  the 
best  of  our  belief  the  mucosa  and  peritoneal  coats  of  the 
stomach  are  almost  or  quite  insensitive  to  all  those  tactile, 
thermal,  chemical,  and  painful  stimuli  which  the  skin  and 
the  mucosa  of  the  mouth  so  readily  appreciate.  The  mus- 
cular coat,  however,  is  appreciative  of  alterations  in  tonic 
or  peristaltic  activity  and  states  of  ‘stretch’,  and  Carlson 
clearly  demonstrated  that  the  hunger  sensation  is  accom- 
panied by  and  synchronizes  with  increased  peristalsis.  With 
exaggerated  degrees  of  muscle-tension  pain  occurs. 

I propose  to  consider  in  turn  hunger-pain,  flatulence, 
heartburn,  acid  regurgitation,  water-brash,  and  hiccups. 
The  first  and  the  third  of  these  are  wholly  sensory  pheno- 
mena. In  the  remainder  there  are  sensory  discomforts  with 
objective  associations.  In  the  last-named  only  are  the 
attendant  discomforts  remote  from  the  upper  alimentary 
tract,  although  this  is  commonly,  if  not  invariably,  their 
seat  of  origin. 


SOME  COMMON  GASTRIC  SYMPTOMS  87 

In  each  case  I shall  discuss  the  nature  of  the  symptom, 
its  common  morbid  associations,  what  we  know  or  can  at 
present  infer  in  respect  of  its  physiology,  and,  lastly,  its 
treatment. 


Hunger-pain 

Hunger-pain  is  felt  in  the  epigastrium.  It  is  usually 
described  as  ‘gnawing’  in  character  or  as  a ‘bad  ache’,  and 
it  is  frequently  associated  with  a sensation  of  sinking, 
hollowness,  or  emptiness.  It  is  fairly  strictly  localized,  but 
occasionally  an  attendant  discomfort  spreads  upwards  into 
the  chest.  It  develops  characteristically  between  two  and 
three  hours  after  the  last  meal,  and  endures  for  an  hour  or 
so  unless  relieved  by  food,  fluid,  or  alkaline  medicines.  Cold, 
fatigue,  mental  worry,  and  tobacco  tend  to  increase  it; 
warmth,  peace  of  mind,  and  holidays  relieve.  It  may  be 
associated  with  water-brash  and  vomiting  and  with  sensa- 
tions of  gastric  flatulence. 

It  is  most  frequently  encountered  in  cases  of  duodenal 
ulcer,  but  occurs  with  some  gastric  ulcers,  and  occasionally 
with  early  growths  of  the  stomach.  It  is  also,  however, 
registered  in  some  cases  of  dyspepsia  due  to  gall-bladder  and 
appendicular  disease,  and,  at  times  of  stress  or  in  association 
with  tobacco-excess  in  patients  endowed  with  the  over- 
active,  over-acid  stomach  which  we  recognize  ns  contribu- 
tory to  the  ulcer-diathesis,  it  may  arise  without  a lesion  of 
any  kind.  The  fact  that  it  may  occur  in  the  absence  of  any 
gastric  or  duodenal  lesion  is  the  best  evidence  that  it  does 
not  express  these  lesions,  but  only  the  nervous  perturbation 
of  function  which  they  arc  liable — as  foci  of  irritation — to 
engender. 

Whether  the  irritation  be  local,  distal,  or  central,  we 
believe  its  effect  to  be  the  production  of  a hj'pertonic 
‘behaviour’  or  ‘posture’ — that  is  to  say,  an  excessive  tonic 
and  peristaltic  activity — in  the  pars  pylorica  shortly  before 
the  stomach  is  due  to  empty.  This  abnormal  increase  in 
muscle  tension  is  the  cause  of  the  pain.  When  food  or  fluid 
is  introduced  into  the  normal  stomach  the  normal  response 
is  a relaxation  of  tension  to  accommodate  the  increased 


83  TIIE  NATURE  AND  RELIEF  OF 

content.  If  this  did  not  occur,  intrngastric  pressure  would 
rise  continually  during  a meal.  The  occurrence  of  this  same 
relaxation  in  disease  cases  the  pain,  which  alternatively 
departs  eventually  when  the  stomach  empties  completely. 
Alkalis,  such  as  bicarbonate  of  soda,  are  believed  to  relax 
the  cardiac  and  pyloric  sphincters  and  so  ease  the  situation 
by  an  expulsion  of  gas  and  a diminution  of  intragastric 
pressure.  At  one  time  hunger-pain  was  regarded  as  a 
symptom  of  hyperchlorhydria,  but  I have  seen  it  in  associa- 
tion with  achlorhydria,  and  many  people  with  hyper- 
chlorhydria never  experience  it. 

The  treatment  of  hunger-pain  includes  the  treatment  of 
the  underlying  cause,  but  suitably  frequent  feeds  and  alkalis 
play  an  important  part  in  all  those  conditions  in  which  the 
cause  cannot  be  eradicated,  and  also  play  their  part  in  pro- 
moting healing  of  ulcers  by  giving  rest  to  the  diseased  part. 

Flatulence 

In  questioning  patients  about  flatulence  we  should  always 
determine  first  of  all  whether  they  mean  stomach-wind  or 
bowel-wind.  I am  here  only  concerned  with  the  former. 
The  symptom  is  characterized  on  the  one  hand  by  sensa- 
tions of  fullness  or  discomfort  of  varying  degree  in  the 
epigastrium  or  chest,  and  on  the  other  by  eructations  of 
gas  or  belching.  The  eructated  gas  is  usually  odourless, 
but  in  certain  conditions  it  may  be  foul.  When  the  smell 
is  of  ‘rotten  eggs’  or  sulphuretted  hydrogen,  gastric  stasis 
with  protein  decomposition  is  always  present,  and  the 
symptom  is  therefore  of  real  diagnostic  value  in  pyloric 
stenosis  or  obstruction.  Very  occasionally  it  is  noted  as  a 
transitory  symptom  in  association  with  an  infective  gastritis. 
Eructations  of  flatus  or  bowel-wind  are  pathognomonic  of 
gastro-colic  fistula,  and  make  the  diagnosis  even  in  the 
absence  of  radiological  proof. 

Odourless  flatulence  is  one  of  the  commonest  symptoms 
of  daily  practice.  It  may  be  due  to  trivial  functional  dis- 
turbances or  serious  organic  disease.  The  sensations  of 
flatulence  may  clearly  be  produced  by  an  actual  excess  of 
air  or  gas  in  a normal  stomach  or  by  a normal  content  in 


SOME  COMMON  GASTRIC  SYMPTOMS  89 

a hypertonic  organ.  There  is  no  good  evidence  that  gas  can 
be  evolved  in  or  diffused  into  the  stomach  sufficiently 
rapidly,  lacking  an  obstructive  lesion,  to  cause  discomfort 
or  repeated  eructations.  Repeated  and  noisy  eructations 
are  always  due  to  air-swallowing,  and  even  the  flatulent 
discomforts  of  organic  disease  arc  commonly  aggravated  by 
this  subconscious  habit. 

Of  organic  lesions  in  which  flatulence  is  a common  com- 
plaint I have  already  mentioned  duodenal  ulcer.  In  gall- 
stones and  cholecystitis  it  is  a more  pronounced  feature, 
and  ‘bursting  flatulence’  is  a frequent  complaint  in  the 
dyspepsias  of  gall-bladder  disease.  Eructation  also  com- 
monly terminates  anginal  attacks  and,  because  of  this, 
anginal  pains  have  often  been  erroneously  attributed  to 
dyspepsia. 

The  habit  of  air-swallowing,  or  acrophagy,  is  initiated  by 
forcible  attempts  to  relieve  a gastric  discomfort  by  eructa- 
tion, the  act  being  preceded  by  gulping  of  air.  This  gulping, 
which  can  be  seen  and  heard  by  any  observant  witness, 
becomes  established  as  a conditioned  reflex  and  may  cause 
years  of  misery.  Air-swallowing  is  sometimes  initiated  by 
the  repeated  swallowing  of  mucus  necessitated  by  pharyn- 
geal catarrh,  and  occasionally  as  an  aftermath  of  ether- 
anaesthesia.  A simple  explanation  and  instructions  to 
avoid  forcible  eructation  may  result  in  dramatic  cures 
where  other  treatments  and  endless  prescriptions  have 
failed,  ns  they  must  fail  in  that  they  take  no  recognition  of 
the  cause  of  the  symptom.  Peppermint  drops  or  bicar- 
bonate of  soda  in  hot  water  help  to  alleviate  transitory  post- 
operative flatulence  and  the  flatulence  due  to  the  disturbed 
gastric  motility  of  organic  disease,  but  even  in  these  cases 
suitable  explanation  plays  its  part. 

JIeABTBUBX 

Heartburn,  one  of  the  commonest,  lias  also  been  one  of 
the  most  elusive,  of  dyspeptic  symptoms.  It  has  also  suffered 
confusion  with  water-brash  and  acid  eructations — two  en- 
tirely distinct  symptoms.  The  sensation  is  characteristically 
one  of  burning  in  the  course  of  the  gullet.  Its  distribution 


00  THE  NATUnn  AND  ItELIEF  OF 

is  vertically  linear,  and  it  may  be  experienced  at  any  level 
between  the  pomum  Adami  and  the  xiphistemum.  It 
changes  its  level  and  fluctuates  in  intensity,  and  may 
endure  for  minutes  or  much  longer  periods.  It  is  not,  as  a 
rule,  accompanied  by  eructations  of  fluid.  It  may  be,  but 
is  not  necessarily,  cased  by  food  or  alkalis.  It  is  not  a 
symptom  of  organic  disease,  but  is  an  association  of  hurry 
and  worry,  of  carbohydrate  excesses,  of  anaemic  dyspep- 
sias, and  (replacing  the  nausea  of  the  earlier  phase)  it  is, 
with  many  women,  a most  troublesome  symptom  in  the 
later  months  of  pregnancy. 

At  one  time  heartburn  was  thought  to  be  a symptom  of 
‘acidity*,  largely  because  alkalis  may  relieve  it,  but  it  can 
occur  in  patients  with  complete  achlorhydria,  and  it  is  not 
a particular  feature  of  dyspepsias  associated  with  hyper- 
chlorhydria. 

By  analog}’  with  other  burning  pains,  such  as  tenesmus, 
we  may  argue  that  it  is  due  to  some  degree  of  tonic  oeso- 
phageal contraction,  and  the  experimental  work  of  W.  W. 
Payne  and  E.  P.  Poulton1  supports  this  hypothesis.  Sodium 
bicarbonate  and  alokol — a proprietary  preparation  of 
aluminium  hydroxide — probably  by  relaxing  the  cardia, 
give  the  best  help,  but  dietetic  adjustments  and  improve- 
ments in  general  and  nervous  health  also  play  their  part. 

Acid  Regurgitation 

This  symptom  describes  itself,  and  is  characterized  by  a 
sudden  regurgitation  into  the  gullet  and  mouth  of  sour 
fluid,  which  may  even  roughen  the  teeth.  It  is  the  only 
direct  symptom  of  gastric  hyperacidity,  and,  even  so, 
occurs  only  in  a limited  proportion  of  patients  with  hyper- 
chlorydria.  The  treatment  is  the  treatment  of  any  under- 
lying cause,  such  as  duodenal  ulcer,  tobacco  excess,  or 
rushed  irregular  meals,  combined  with  alkaline  therapy. 

Water-brash 

By  water-brash  we  imply  the  sudden  arrival  in  the  mouth 
and  gullet  of  large  quantities  of  clear,  tasteless,  watery 

1 Quarterly  Joum.  Med.,  1023,  xvii.  53. 


SOME  COMMON  GASTRIC  SYMPTOMS  01 

secretion.  It  is  to  be  distinguished  from  the  excessive 
and  stringy  mucoid  secretion  of  alcoholic  oesophagitis  and 
some  oesophageal  obstructions.  It  occurs  more  frequently  in 
duodenal  ulcer  than  any  other  dyspeptic  disease,  and  may, 
perhaps,  be  regarded  as  an  exaggeration  of  the  ‘mouth- 
watering’ which  is  proverbially  associated  with  hunger,  but 
better  manifest  in  dogs  than  men.  It  is  synchronous  with 
the  ‘hunger-pain’,  is  due  to  a sudden  secretion  of  saliva,  and 
possibly  has  a protective  purpose,  for,  if  swallowed,  it  may 
even  relieve  the  pain.  Pain  in  the  parotids  sometimes  accom- 
panies this  sudden  salivary  hypersecretion. 

Hiccups 

Hiccups  are  usually  due  to  trivial  causes  and  regarded  ns 
a domestic  joke.  When,  however,  they  occur  in  old  people 
and  arc  long  continued  they  may  cause  serious  exhaustion 
and  the  gravest  anxiety.  They  may  also  be  of  evil  import 
as  accompaniments  of  acute  abdominal  catastrophes  and 
uraemia.  In  children  they  are  particularly  frequent  and 
innocent,  and  probably  to  be  related  to  bolting  of  food 
and  starch-excess.  Some  people  are  unable  to  take  very  hot 
or  peppery  soup  without  immediate  hiccups.  They  are  a 
fnmiliar  manifestation  of  an  alcoholic  bout.  In  all  of  these  it 
must  be  assumed  that  the  symptom  is  a reflex  consequence 
of  gastric  irritation.  Its  mechanism  would  seem  to  include 
a sudden  closure  of  the  glottis  in  inspiration,  with  a simul- 
taneous ‘ twitch  or  arrest  in  its  descent,  of  the  diaphragm. 
In  the  abdominal  catastrophes  the  stomach  is  usually 
dilated,  and  filled  with  turbid  brownish  fluid  and  sometimes 
regurgitated  intestinal  contents.  In  uraemia,  either  uraemic 
gastritis  or  a nervous  intoxication  might  be  invoked.  There 
arc  also  occasional  epidemics  of  hiccups,  and  one  followed 
or  nccompanicd  the  wave  of  encephalitis  lethargica  shortly 
after  the  First  World  War,  although  there  was  no  final  proof 
that  it  was  due  to  the  same  cause. 

In  their  graver  forms  hiccups  are  most  intractable. 
Gastric  lavage  in  cases  of  dilated  stomach  may  put  a 
stop  to  them.  In  the  unexplained  and  long-continued 
hiccups  of  old  people,  and  occurring  nt  any  age  in  the 


02  THE  NATURE  AND  RELIEF  OK  GASTRIC  SYMPTOMS 
epidemic  variety,  it  is  customary  to  try  oil  of  cajuput  or 
tincture  of  iodine  by  the  mouth,  but  they  are  usually 
ineffectual.  An  ice-cold  application  to  the  epigastrium 
sometimes  succeeds.  The  induction  of  violent  sneezing  (not 
applicable  in  abdominal  cases  or  the  presence  of  exhaustion) 
is  a remedy  as  old  as  the  Socratic  Dialogues,  and  is  some- 
times most  effective.  Stronger  remedies  may,  however,  be 
necessary,  not  excluding  heroin  and  morphine,  and  even 
with  these  the  spasms  may  continue  during  sleep. 

Conclusion 

What  do  we  gain  from  a fuller  understanding  of  these 
familiar  symptoms?  First  of  all  we  gain  a better  precision 
in  diagnosis  and  improve  our  aptitude  for  early  diagnosis. 
Our  dependence  upon  objective  measures  and  the  accessory 
aids  of  the  X-ray  department  and  the  laboratory  is  dimin- 
ished. The  stories  of  our  patients  develop  a meaning  which 
they  previously  lacked,  and  a practical  morbid  physiology, 
even  though  it  stand  in  need  of  other  proofs,  adds  interest 
to  our  handling  of  disorders  which  have  the  reputation  of 
being  rather  dull  or  difficult.  Finally  we  come  to  rely  more 
upon  simple  explanations  and  reasoned  regimes  and  less 
upon  the  eternal  bottle  of  bismuth  and  soda,  which,  valuable 
though  it  be  in  some  conditions,  has  no  right  to  be  regarded 
as  a panacea  for  all  digestive  ills. 

A similar  attention  to  detail  in  considering  the  symptoms 
of  cardiovascular,  respiratory,  and  other  diseases  is  similarly 
rewarded.  Let  us  therefore  endeavour  to  remain  constantly 
curious  about  the  nature  and  meaning  of  every  symptom 
which  our  patients  bring  to  us. 


VII 

THE  NATURAL  HISTORY  OF  DUODENAL  ULCER1 

The  subject  of  this  lecture  is  one  which  has  engaged  the 
thoughts  of  physicians  and  surgeons  for  a quarter  of  a cen- 
tury, but  which  still  supplies  them  with  unsettled  problems. 
Mindful  of  the  title  of  this  office  and  of  my  inability  to 
expound  the  anatomical  or  the  surgical  precepts  of  John 
Hunter,  I have  felt  that  I might  at  least,  in  humble  fashion, 
demonstrate  my  devotion  to  the  observational  method  of 
John  Hunter  the  naturalist.  The  physician  is  or  should  be, 
above  all,  a student  of  the  natural  origins,  associations,  and 
sequences  of  disease,  and  in  this  capncity  he  can  best  render 
his  contribution  to  prognosis  and  to  therapeutic  principle. 

During  the  past  twelve  years  I have  had  considerable 
opportunities  of  studying  the  problems  of  duodenal  ulcer 
both  at  hospital  and  in  the  course  of  private  practice.  My 
close  association  with  Sir  Arthur  Hurst  and  his  thorough 
methods  of  inquiry  has  furnished  a constant  stimulus,  and 
I have  been  indebted  to  my  friends,  the  surgeons  and  the 
radiologists,  for  much  instruction.  Increasing  familiarity 
with  the  disease  has  bred  anything  but  contempt.  Each 
year  there  have  been  new  observations  to  record  and  new 
explanations  to  seek.  The  vast  fund  of  information  in  the 
literature  and  the  steady  output  of  special  researches  on 
the  subject  notwithstanding,  a broad  review  of  the  natural 
history  of  ulcus  duodeni  is,  I believe,  justified  by  the  follow- 
ing four  considerations: 

1.  Duodenal  ulcer  is  a prevalent  disease,  and  there  is  evi- 
dence (although  due  allorcance  must  be  made  for  growth 
and  concentration  of  population  and for  improvements  in 
diagnosis)  that  this  prevalence  waxes  rather  than  wanes 
under  the  existing  conditions  of  civilized  life. 

An  inquiry  into  the  admission-rates  of  some  common 
diseases  at  Guy’s  Hospital  shows  that,  on  the  average,  100 

1 Hunterian  lecture  delivered  before  the  1 loyal  College  of  Surgeons, 
5 February  1932  (The  Lancet,  1932, 1.  327). 


01  Tire  NATURAL  HISTORY  OF  DUODENAL  ULCER 
cases  of  duodenal  ulcer  are  admitted  annually-— that  is  to 
say,  about  1 per  cent,  of  all  admissions — a figure  somewhat 
less  than  the  admission-rate  for  tuberculosis  (all  forms)  but 
greater  than  that  for  all  the  pleurisies  and  lobar  pneumonias 
combined.  In  addition,  large  numbers  of  cases  are  treated 
in  the  Out-Patient  department  In  my  private  practice, 
which  has  a general  character— albeit  with  an  abdominal 
bias — ’the  ten  most  frequent  diagnoses  arc  duodenal  ulcer, 
anxiety  state,  constipation,  cholecystitis  and  gall-stones, 
hyperpicsia  (with  its  cardiac  and  neurological  sequels), 
tuberculosis,  anaemia  (all  forms),  migraine,  spastic  colon, 
and  obesity.  Of  these,  duodenal  ulcer  heads  the  list,  ac- 
counting for  approximately  5 per  cent,  of  all  my  cases. 

Wilkie  [1],  stressing  the  stendy  increase  in  the  cases  of 
perforation  at  the  Royal  Infirmary,  Edinburgh,  in  spite  of 
improvements  in  diagnosis  and  treatment  and  a multiplica- 
tion of  the  smaller  hospitals  capable  of  dealing  with  these 
catastrophes,  reasonably  argues  that  the  total  incidence  of 
the  disease  is  rising.  At  Guy’s  Hospital  the  same  thing  is  to 
be  observed.  Dividing  the  period  1910-29  into  four  five- 
year  periods  the  admission-rates  for  perforated  duodenal 
ulcer  were  ns  follows: 

1010-li  . 48  cases 

1015-10  (war  period)  . 20  „ 

1020-1  ....  87  .. 

1025-0  115  „ 

A part  of  this  increase  may  be  due  to  the  fact  that  sur- 
geons have  come  to  observe  a better  precision  in  locating 
ulcers  with  reference  to  the  pyloric  sphincter.  The  annual 
total  of  deaths  from  duodenal  ulcer  in  England  and  Wales 
has  almost  doubled  in  the  last  decade  (see  below).  It  seems 
doubtful  whether  this  increase  can  be  wholly  accounted  for 
by  such  factors  as  growth  of  population,  improved  recogni- 
tion, and  better  habits  of  precision  in  recording  the  site  of 
the  ulcer.  Moreover,  the  deaths  from  gastric  ulcer  have 
shown  a contemporary  and  parallel  rise.  In  both  eases  the 
increase  is  much  more  conspicuous  in  the  males. 

2.  Although  the  mortality  of  its  most  serious  complication 
has  been  remarkably  diminished  by  surgery,  duodenal 


THE  NATURAL  HISTORY  OP  DUODENAL  ULCER  05 
ulcer  continues  to  take  its  toll  and  remains,  through  pain- 
ful dyspepsia  and  occasional  haemorrhage,  a serious 
cause  of  disability  and  lost  efficiency  among  members  and 
classes  of  the  community  often  endowed  with  energy  and 
usefulness  above  the  average  and  sometimes  with  out- 
standing ability. 

8.  Although  of  all  the  dyspeptic  disorders  duodenal  ulcer 
presents  the  most  clcar-cut  clinical  picture,  its  leading 
characters  and  natural  behaviour  are  not  so  widely 
appreciated  in  the  profession  as  they  might  be. 

Thus  the  length  of  time  elapsing  between  first  appearance 
of  symptoms  and  diagnosis  is  usually  to  be  reckoned  in  years 
rather  than  months.  As  the  prospects  of  sound  healing  with 
a medical  regime  arc  best  in  the  early  days  and  diminish 
with  the  passage  of  time  (vide  Nielsen  [2],  whose  figures 
support  the  common  experience  of  physicians),  the  prompt 
recognition  of  symptoms  is  an  essential  contribution  to 
therapeutics.  Except  in  the  case  of  doctors  or  medical 
students,  I rarely  see  a case  with  a history  of  only  weeks  or 
months.  Among  184  cases  of  duodenal  ulcer  referred  to  me 
in  which  the  length  of  history  is  recorded,  there  were  only 
52  in  which  this  was  two  years  or  Jess.  I have  notes  of  48 
cases  with  histories  of  10  years  and  upwards,  and  of  these 
17  gave  histories  of  20  years  or  more,  and  a furthers  had  had 
symptoms  for  at  least  80  years.  Among  121  cases  (excluding 
cases  of  pyloric  stenosis)  in  which  the  length  of  time  between 
first  symptoms  and  diagnosis  could  be  roughly  computed 
(all  cases  diagnosed  in  less  than  one  year  being  counted  as 
‘immediate’)  the  average  interval  was  seven  years. 

4.  Duodenal  ulcer  has  supplied  us  with  a number  of  prob- 
lems in  aetiology,  prognosis,  and  treatment  which  are  at 
present  only  partially  solved . 

Doubts  and  difficulties  continue  to  confront  us.  The 
wavering  from  medical  to  surgical  and  bock  to  medical 
opinion,  and  the  continued  invention  of  new  treatments  and 
operations,  are  eloquent  of  our  uncertainty.  Extravagant 
claims  have  been  made  from  time  to  time  by  protagonists 
of  both  the  medical  and  surgical  schools.  Bacteriology, 
biochemistry,  minute  anatomy,  and  statistical  inquiry  have. 


on  Tins  NATURAL  HISTORY  OF  DUODENAL  ULCER 
severally  and  collectively,  failed  to  give  the  whole  answc 
to  our  question-  We  have  reached  a point  at  which  there 
peutic  experiment  and  specialized  studies  seem  no  mor 
competent  to  give  help  in  practice  than  a general  survey  c 
the  active  disease  ns  it  occurs  and  ns  it  varies  in  living  mar 

To  achieve  such  a survey  with  any  completeness  am 
within  the  compass  of  a single  lecture  would  bean  impos 
siblc  task.  I must  therefore  content  myself  with  a condensa 
tion  of  experience  and  must  ask  to  be  excused  lengthy  refer 
ences  to  the  literature.  All  that  is  best  of  our  knowledge  o 
the  subject  is  to  be  found  in  Moynihan’s  Duodenal  Ulcer  anc 
in  Gastric  and  Duodenal  Ulcer  by  Hurst  and  Stewart.  T< 
the  authors  of  these  classics  we  must  always  remain  in' 
debted.  If  my  remarks  provide  some  small  stimulus  to  tht 
further  pursuit  of  the  old  observational  method  (and  with- 
out the  co-operation  of  this  method  experimental  medicint 
can  make  but  a halting  advance),  and  if,  in  addition,  I car 
adduce  reasons  for  the  adoption  of  a more  judicial  attitude 
in  arranging  the  treatment  ot cases,  1 shall  be  well  satisfied . 

I have  among  my  fdes  the  notes  of  upwards  of  350  cases 
interrogated  and  examined  by  myself  to  which  the  diagnosis 
of  duodenal  ulcer  is  attached.  From  these  I have  separated 
for  analysis  only  those  in  which  the  clinical  story  was  con- 
firmed by  operation,  haemorrhage  (generally  mclaena),  or 
a reliable  radiologist.  This  series  comprises  (a)  218  cases, 
of  which  24  had  proceeded  to  the  development  of  pyloric 
stenosis.  To  these  I have  added  ( b ) 35  cases  of  anastomotic 
ulcer,  and  (c)  8 cases  of  other  surgical  disappointments  fol- 
lowing gastro-jejunostomy  undertaken  for  the  relief  of  a 
duodenal  ulcer.  My  mental  images  are  naturally  coloured  by 
an  equivalent  experience  of  hospital  patients  drawn  from 
other  sections  of  the  community,  but  I have  preferred  to 
employ  the  material  immediately  to  my  hand  and  upon 
which  all  observations  were  intimate  and  personal. 

TnE  Origins  of  Duodenal  Ulcer 
Constitution 

Wherein  should  we  seek  the  beginnings  of  a disease  which 
tends  strongly  to  relapse  or  chronicity  and  which  has  no 


HIE  NATURAL  HISTORY  OF  DUODENAL  ULCER  97 
basis  in  contagion  or  epidemic  causes  ? Clearly,  I think,  in 
the  peculiarities  and  antecedents  of  its  victims  or  in  their 
habits  and  environment.  Preoccupied  with  the  lesion  and 
with  hypotheses  as  to  its  mode  of  initiation  and  perpetua- 
tion by  local  bacterial  and  chemical  action  we  have  too  long 
delayed  our  study  of  the  soil  in  which  it  thrives.  \Vc  have 
but  to  observe  in  sufficient  number  our  patients  as  they 
come  before  us  to  appreciate  that  we  are  here  confronted 
with  distinctive  human  types  or  constitutions.  Within  these 
constitutions  we  may  already'  discern  certain  physical,  bio- 
chemical and  psychological  variants  which  between  them 
supply  what  we  may  call  the  ‘ulcer  diathesis’.  Thus,  if  our 
notes  are  sufficiently  descriptive,  we  find  again  and  again 
that  our  patients  are  delineated  as  ‘lean  and  nervous’  men, 
often  tense  and  muscular  and  with  brisk  mental  and  physical 
reactions,  or,  alternatively,  as  robust  and  energetic  and, 
when  free  from  symptoms,  of  strikingly  healthy  appearance. 
There  are  even  physiognomical  characters  which  may  impel 
us  to  hazard  the  diagnosis  before  the  history  is  taken,  but, 
as  the  disease  itself  may  put  a stamp  upon  the  features,  we 
cannot  here  he  sure  that  we  arc  concerned  with  heritable 
variations.  The  epigastric  angle  is  commonly  wide,  and  the 
observations  of  Faber  [8]  have  enabled  us  to  correlate  this 
feature  with  the  short,  high,  ‘stcerhom’  stomach  of  the 
radiologist.  Moody,  Van  Nuys,  and  Chamberlain  [4]  find 
this  type  of  stomach  more  common  in  the  male  sex.  Camp- 
bell and  Conybcarc  [5]  have  also  associated  this  type  of 
stomach  with  broad,  athletic  men  on  the  one  hand  and  with 
hypcrchlorhydria  on  the  other.  Izod  Bennett  [0]  and  I 
earlier  reported  hyperchlorhy'dric  curves  in  8 per  cent,  of 
healthy  male  students.  Psychologically  these  folk  arc  ener- 
getic, restless,  conscientious,  intent  on  their  projects,  and 
not  seldom  given  to  anxiety  of  mind.  If  engaged  in  business 
their  city  lunch  is  an  occasion  not  for  respite  and  digestion, 
but  for  more  business.  Recognition  of  these  facts  is  essen- 
tial to  a proper  understanding  of  the  disease,  and  to  the 
handling  of  cases.  No  disease,  however,  should  be  sum- 
marily' ascribed  in  any  part  to  constitutional  causes  unless 
we  can  also  demonstrate  that  it  exhibits  a familial  tendency'. 

H 


08  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER 
Other  chronic  maladies  like  gou  t,  asthma,  and  epilepsy  have 
long  been  accepted  as  having  some  basis  in  constitutional 
causes  and  provide  positive  family  histories  in  approxi- 
mately 25  per  cent  of  cases.  Occasional  reports  on  the  fami- 
lial tendency  of  ulcer  had  appeared  previously,  but  it  was 
not  until  1921  that  Hurst  [7, 8],  who  is  so  largely  responsible 
for  our  reawakened  interest  in  the  constitutional  factor,  laid 
emphasis  upon  the  real  importance  of  inheritance  in  this 
disease.  In  his  paper  bearing  on  the  subject  he  quoted  among 
others  three  family  histories  which  had  then  come  to  my 
notice,  including  one  in  which  tlircc  brothers  were  operated 
on  for  duodenal  ulcer  and  a sister  for  gastric  ulcer.  In  my 
present  series  (a)  there  were  23  instances  (10  per  cent.)  in 
which  a near  relative — i.e.  parent,  child,  brother,  sister, 
aunt,  uncle,  or  first  cousin — was  recorded  as  having  had  a 
duodenal  ulcer.  In  one  instance  the  father  of  the  patient, 
two  uncles,  and  one  cousin,  and  in  another  a sister  and  two 
maternal  cousins  had  been  afflicted.  Historiesof ‘dyspepsia* 
in  near  relatives  are  also  common.  If  allowance  be  made  for 
the  infrequent  recognition  of  duodenal  ulcer  as  a cause  of 
dyspepsia  in  the  last  and  preceding  generations,  the  fre-. 
quency  with  which  the  diagnosis  is  missed  at  the  present 
day,  the  customary  inattention  to  the  family  history  of  a 
disease  until  its  importance  becomes  widely  accepted,  and 
the  difficulty  always  experienced  in  collecting  and  recording 
medical  pedigrees,  it  seems  probable  that  the  actual  inci- 
dence of  positive  family  histories  in  duodenal  ulcer  would 
prove  to  be  higher  than  these  figures  indicate.1 

SexjAgc,  and'Jiccupalion 

Sex. — The  well-recognized  preponderance  of  male  over 
female  cases  (four  to  one  in  the  present  series)  must  also 
have  some  bearing  on  aetiology.  The  broad  epigastric  angle 
and  steerhom  stomach  are  commoner  in  the  male  sex.  The 

1 Since  this  lecture  was  penned  I have  encountered  jet  another  'ulcer 
family’,  illustrating  the  Bad  consequences  of  an  intermarriage  between  pre- 
disposed stocks:— Father  D.U.;  Mother  C.U.;  three  sons  D.U.;  one 
daughter  'ulcer  symptoms';  her  son  perforated  D.U.  and  her  daughter 
peptic  ulcer.  One  paternal  cousin  in  the  middle  generation  D.U. 


THE  NATURAL  HISTORY  OF  DUODENAL  ULCER  00 
male  of  the  type  described  spends  his  energies  freely,  often 
bolts  or  misses  meals,  often  smokes  excessively,  and  gener- 
ally lacks  the  aptitude  or  opportunity  for  mental  quietude  in 
his  life  which  falls  more  frequently  to  the  lot  of  woman-kind. 

Age. — The  age-incidence  of  the  disease  is  also  instructive. 
Roughly  half  the  cases  arc  between  the  ages  of  30  and  50, 
that  is  to  say,  within  the  period  of  life  when  work  and  worry 
most  predominate.  Duodenal  ulcer  is  rare  in  childhood  and, 
in  fact,  until  after  puberty,  although  occasional  boyhood 
cases  arc  to  be  found  in  any  long  scries.  It  is  rare  for  symp- 
toms to  make  their  first  appearance  after  the  sixth  decade, 
although  recurrences  then  and  even  into  the  seventies  and 
eighties  arc  not  infrequent.  The  average  age  in  my  scries  at 
the  time  of  consultation  (excluding  cases  of  pyloric  stenosis) 
was  47  years.  The  youngest  patient  was  nged  19,  the  oldest 
83.  The  youngest  calculated  age  of  onset  was  9 years,  and 
there  were  others  as  young  as  12  and  15.  Positive  family 
histories,  as  we  should  anticipate,  appear  to  be  more  fre- 
quent in  the  youthful  group. 

Occupation. — The  influence  of  occupation  is  hard  to  assess. 
No  figures,  for  instance,  are  available  for  comparing  the 
incidence  of  the  disease  in  urban  and  agricultural  com- 
munities. On  a retrospect  of  experience  it  is  difficult  to 
avoid  the  conclusion  that  the  life  and  occupations  of  the 
city  arc  more  productive  of  the  disease.  Among  91  cases 
in  which  the  profession  is  recorded  I find  28  doctors,  22 
business  men  and  lawyers,  18  officers  of  the  Army,  Navy, 
and  Air  Force,  7 dentists,  and  21  in  other  walks  of  profes- 
sional life.  Doctors  and  members  of  the  fighting  forces  nlso 
appear  to  show  a special  liability  according  to  Hurst’s 
figures  from  New  Lodge  Clinic  [8].  The  missed  and  bolted 
meals,  and  the  cares  which  come  to  interrupt  the  smooth 
course  or  his  digestion,  might  well  be  advanced  in  part  ex- 
planation of  the  medical  man’s  apparent  predisposition  to 
the  disease.  Its  occurrence  in  the  Services  is  merely  a re- 
minder that  the  disease  is  one  of  robust  or  active  rather 
than  frail  or  indolent  constitutions.  Lord  Moynihan  [9]  has 
recently  referred  to  his  experience  or  awes  in  athletes  of  the 
first  rank. 


100  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER 
Other  Actiological  Factors 

Tobacco. — Smoking  had  been  indulged  in  by  the  men 
almost  invariably  and  sometimes  in  great  excess,  but 
although  medical  and  surgical  opinion  unite  in  opposing 
the  free  use  of  tobacco  by  ulcer  victims,  and  many  patients 
appreciate  that  they  arc  better  without  it,  or  even  that  it 
may  aggravate  symptoms,  it  is  difficult  to  obtain  concise 
proofs  with  regard  to  the  part  which  this  habit  plays  in 
determining  the  arrival  or  perpetuation  of  symptoms  or  the 
different  incidence  of  duodenal  ulcer  in  the  two  sexes. 

Focal  Sepsis. — Although  it  is  a reasonable  part  of  treat- 
ment to  eradicate  focal  sepsis,  and  although  the  teeth  or  the 
appendix  can  often  be  shown  to  he  unhealthy,  the  actual 
contribution  of  cryptic  infections  is  still  difficult  to  assess. 
Dental,  tonsillar,  and  sinus  infections  are  not  necessarily 
followed  by  duodenal  ulceration,  even  in  persons  predis- 
posed by  constitution  or  habits  of  life.  Furthermore,  duo- 
denal ulcer  may  develop  in  patients  in  whom  no  focus  can 
be  found  or  who  have  long  since  been  deprived  of  their 
teeth  or  vermiform  appendix. 

Environment. — I have  referred  to  the  possibility  of  a 
higher  incidence  of  duodenal  ulcer  under  the  conditions  of 
life  in  cities.  With  others  I have  also  been  struck  by  the 
promptly  beneficent  influence  of  a healthy  out-of-door  life 
on  the  active  symptoms  of  the  disease.  A country  holiday 
will  frequently  cut  short  an  attack.  Nervous  influences 
play  their  part,  for  pain  may  cease  on  the  first  day  of  the 
holiday.  One  patient  of  mine  could  spend  weeks  ski-ing  in 
the  Austrian  Alps,  living  on  black  bread  and  beer,  without 
symptoms,  but  would  relapse  in  his  English  home  where  his 
diet  was  carefully  arranged.  But  more  impressive  than  such 
isolated  cases  has  been  the  story,  repeated  to  me  on  several 
occasions,  that  men  with  duodenal  ulcer,  who  were  dyspep- 
tics before  their  military  service  and  again  on  their  return  to 
office  life,  were  entirely  free  from  symptoms  under  the  hard 
physical  conditions  of  active  service  abroad  during  the  war. 

Climate  may  also  play  some  part.  I have  had  patients 
who  were  free  from  symptoms  in  India  but  afflicted  when 


TIIE  NATURAL  HISTORY  OF  DUODENAL  ULCER  1D1 
at  home,  and  Col.  E.  B.  Marsh,  A.M.S.,  -who  made  a particular 
study  of  duodenal  ulcer  among  the  troops  at  Aldershot, 
where  he  found  it  prevalent,  later  wrote  to  me  from  India  to 
report  that  in  twenty-two  months  in  the  East  among  British 
troops,  differing  only  in  that  they  were  slightly  older  than  the 
home  troops,  he  had  not  seen  a single  proven  case  of  ulcer. 

Season,  as  Moynihan  [10]  showed  long  since,  undoubtedly 
influences  the  fluctuations  of  the  disease  in  the  individual, 
winter,  or  autumn  and  spring  recurrences  being  commonly 
described.  Recurrences  at  these  seasons  or  ‘in  cold  weather’ 
were  specifically  entered  in  my  notes  in  25  cases  (12  percent, 
of  the  duodenal  ulcer  series  (a)).  Raw  cast  winds  are  parti- 
cularly obnoxious  to  sufferers  from  duodenal  ulcer.  Sea- 
sonal infections  may  be  a factor,  but  the  majority  of 
patients  do  not  remark  on  this  association. 

Mental  States. — A restless  stomach  accompanies  a rest- 
less mind.  In  many  cases  anxiety  and  mental  conflict  seem 
to  play  a part  in  the  aggravation  of  symptoms.  In  a minor- 
ity of  cases  (although  it  be  beyond  proof)  it  is  tempting  to 
wonder  whether  the  disease  would  have  developed  in  the 
absence  of  psychological  turmoil. 

Actiological  studies  arc  thus  shown  to  be  of  some  impor- 
tance, and  if  we  can  cast  our  vision  forwards  to  a time  in 
which  we  shall  be  more  concerned  with  the  prevention  than 
with  the  cure  of  chronic  diseases  of  this  class,  it  is  clear  that 
our  method  will  find  its  basis  quite  as  much  in  intimate 
studies  of  constitution,  habits  of  life,  occupation,  and  en- 
vironment as  in  the  refinements  of  chemistry,  bacteriology, 
and  animal  experiment.  In  our  choice  of  treatment  of  the 
active  disease  we  must  also  remain  attentive  to  these 
elements  in  its  natural  history,  remembering  that  the 
success  of  therapeutic  experiment  in  the  long  run  depends 
even  more  upon  knowledge  and  judgement  than  upon 
technique. 

The  Course  of  Duodenal  Ulcer 
I have  referred  to  the  long  interval  which  commonly 
elapses  between  first  symptoms  and  diagnosis.  The  chief 
reason  for  this  is  to  be  found  in  the  natural  tendency  to 


102  Tin:  NATURAL  HISTORY  OF  DUODENAL  ULCER 
spontaneous  remissions  of  symptoms.  Patients  and  doctors 
alike  in  the  first  attack,  delighted  by  the  quick  response  to 
dietary  care  or  * a bottle  of  bismuth’,  with  disappearance  of 
all  pain  within  a period  of  two  or  three  weeks  or  less,  are 
lulled  into  an  attitude  of  false  security  and  deem  the  ‘bout 
of  indigestion  * past  and  done  with.  As  Moynihan  and  others 
have  clearly  proclaimed,  this  behaviour  is  characteristic  of 
the  disease.  If  we  arc  to  judge  by  the  early  clinical  course 
of  duodenal  ulcer  (for  symptoms  surely  bear  some  relation- 
ship to  ‘activity’)  there  must  be  repeated  attempts  at 
natural  healing,  and  this  is  a particular  justification  for 
medical  measures  at  this  stage.  That  spontaneous  healing 
occurs  is  evident  from  the  scars  found  in  the  course  of 
routine  post-mortem  work.  The  first  attacks  may  last  no 
more  than  ten  days  and  rarely  more  than  three  or  four 
weeks,  and  they  may  be  followed  by  free  intervals  of  enjoy- 
able health,  with  ability  to  cat  all  foods,  enduring  for  six 
months  or  longer.  The  man  who  starts  his  illness  with  a 
melaena  is  really  a lucky  man,  for  by  this  means  his  diagnosis 
is  declared  and  early  and  strict  treatment  instituted.  3fany 
patients  go  free  all  the  summer  months  and  suffer  relapses 
between  October  and  March.  With  the  passage  of  years  the 
bouts  of  dyspepsia  become  more  prolonged  and  frequent. 
And  so  the  disease  may  drag  on  intermittently  for  five,  ten, 
or  even  twenty  years,  with  or  without  distinctive  complica- 
tions and  often,  in  the  latter  event,  without  a diagnosis. 

Haemorrhage  occurred  at  one  stage  or  another  in  rather 
less  than  40  per  cent,  of  this  series  (a),  but  it  should  be  re- 
called that  many  cases  unconfirmed  by-  operation.  X-rays, 
or  haemorrhage  were  excluded,  so  that  the  figure  is  clearly 
too  high.  Most  authors  of  experience  record  haemorrhage 
as  occurring  in  approximately  25  per  cent,  of  cases.  Allow- 
ing for  the  many  1 missed  ’ dyspeptic  cases,  all  recorded  per- 
centage figures  for  the  complications  must  be  accepted 
ns  too  liberal.  Perforation  (including  ‘local  perforations’) 
occurred  in  10  cases  of  the  duodenal  ulcer  series  (a),  and  in 
the  anastomotic  ulcer  series  (b)  (35  cases)  in  7 cases  before 
and  3 after  operation.  These  figures  give  no  indication  of 
actual  frequency  of  perforation.  The  physician  is  rarely 


THE  NATURAL  HISTORY  OF  DUODENAL  ULCER  103 
called  to  these  emergencies.  It  is,  however,  a much  rarer 
complication  than  haemorrhage.  Pyloric  stenosis  occurred 
in  21  (11  per  cent.)  of  my  cases,  series  (a).  The  serious  com- 
plication of  involvement  of  the  head  of  the  pancreas,  with 
its  particular  syndrome  (to  be  described  later),  occurred  in 
2 per  cent,  of  this  series. 

Mortality  of  Duodenal  Ulcer 
It  is  impossible  to  estimate  the  death-rate  of  a disease  so 
widespread  and  yet  so  ill  recorded  as  duodenal  ulcer.  Even 
allowing  that  the  majority  of  deaths  among  patients  of  the 
hospital  class  occur  in  hospital,  wc  can  obtain  no  accurate 
measure,  for  hospitals  not  only  attract  the  eases  of  per- 
foration and  haemorrhage  in  undue  proportion,  but  also 
admit  only  the  more  serious  of  the  dyspeptic  cases.  In 
twenty  years  at  Guy’s  Hospital  there  have  been  153  deaths 
among  cases  of  duodenal  ulcer.  Of  these,  70  followed  per- 
foration, 25  followed  haemorrhage,  and  the  remainder  were 
indexed  ns  due  to  various  secondary  complications  of  per- 
foration or  of  operation  undertaken  for  the  relief  of  the 
disease  or  of  its  complications,  or  to  intcrcurrent  disease. 
That  is  to  say,  in  a hospital  admitting  about  100  cases  a year, 
about  7 or  8 cases  a year  die  from  all  causes.  For  every  one 
of  these  100  cases  admitted  to  the  wards  there  must  be 
several  others  from  the  same  communities  treated  ns  out- 
patients and  in  their  homes,  or  remaining  undiagnosed  and 
untreated.  In  general,  although  its  interruptions  to  health 
arc  numerous,  the  menace  to  life  of  a duodenal  ulcer  is 
not  n very  grave  one.  According  to  the  Registrar-General’s 
returns  there  were  1,140  deaths  (male)  and  ICO  deaths 
(female)  from  duodenal  ulcer  in  England  and  Wales  during 
1030,  as  compared  with  552  (male)  and  129  (female)  in  1920. 
These  figures  arc  sufficiently  arresting,  and  yet  they  must 
represent  but  a small  percentage  or  the  total  army  of  recog- 
nized and  unrecognized  cases. 

Tjif.  Symptoms  of  Duodenal  Ulcer 
Moynihan  [10]  has  rightly  insisted  on  the  nnamnesis  ns 
the  main  plank  in  the  diagnosis  of  duodenal  ulcer.  This 


lot  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER 
should  include  all  proper  inquiries  into  personal  and  family 
history,  environment,  occupation,  and  habits,  for  these 
may  serve  not  only  to  complete  the  opinion,  but  also  to 
balance  judgement  in  therapeutic  decisions.  But  above  all 
our  interrogations  must  deal  intimately  with  subjective 
phenomena.  In  the  majority  of  cases  it  should  be  possible 
to  arrive  at  a diagnosis  of  duodenal  ulcer  from  the  history 
and  sj-mptoms  alone,  and  before  the  physical  examination 
or  accessory  measures,  such  as  radiology  and  the  test-meal, 
have  been  called  upon  to  play  their  part. 

The  leading  symptom  is  the  pain.  It  is  true  that  an  ulcer 
may  be  present  to  the  tune  of ‘wind’  or  ‘acid  vomiting'  and 
that  the  patient  may  deny  the  occurrence  of  true  pain,  but 
this  is  not  usual.  Employing  a method  of  pain-analysis 
which  I have  previously  described  we  may  consider  the  pain 
of  duodenal  ulcer  under  ten  headings,  having  reference  to 
(1)  character;  (2)  severity ; (3)  situation ; (-1)  localization  (or 
extent  of  diffusion);  (5)  paths  of  reference;  (6)  duration; 
(7)  frequency;  (8)  special  times  of  arrival;  (9)  and  (10) 
aggravating  and  relieving  factors.  The  character  of  the  pain 
is  described  with  great  consistency  as  ‘gnawing’  or,  alterna- 
tively, ns  ‘aching’  or  ‘like  a toothache’.  There  is  no  inter- 
mission, although  there  may  be  slight  fluctuations  while  it 
lasts.  It  is  ‘wearing’  and  ‘worrying’  but  not  so  severe,  as  a 
rule,  as  to  prohibit  work,  although  it  may  hamper  efficiency 
and  concentration.  With  the  occasional  complication  of  pan- 
creatic erosion  it  may,  however,  become  very  severe  and  even 
require  morphine  for  its  relief.  Its  situation  is  indicated 
by  the  patient  with  the  finger-tips  in  mid-epigastrium  or 
slightly  to  the  right  in  more  chronic  cases ; it  is  then  gener- 
ally at  a lower  level  than  that  indicated  by  the  right  sub- 
costal gesture  of  cholecystitis.  It  has  a precise  position  and 
localization,  but  in  severe,  old-standing  cases,  and  especially 
when  flatulence  with  nerophagy  is  pronounced,  it  may 
‘spread’  widely  into  the  chest.  When  the  pancreas  is 
involved  it  ‘goes  through’  to  the  back  at  the  same  level  and, 
occupying  the  region  of  the  twelfth  rib  (appreciably  lower 
than  the  subscapular  reference  of  gall-bladder  disease),  it 
may  even  create  a suspicion  of  a right  renal  lesion.  In  these 


THE  NATURAL  HISTORY  OF  DUODENAL  ULCER  105 
cases,  too,  the  anterior  pain  may  be  ‘right  subcostal’  rather 
than  ‘ epigastric’.  The  pain  is  absent  on  waking,  and  remains 
in  abeyance  until  some  two  to  two  and  a half  hours  after 
breakfast.  Arriving,  let  us  say,  at  11.30  a.m.  it  will  persist 
for  an  hour  or  more  until  relieved  by  lunch,  but  it  may 
return  again  before  tea  and  again  in  the  evening.  Rearrange- 
ments of  diet  or  meals  will  modify  the  behaviour  of  the  pain. 
In  cases  of  long  standing  a special  time  of  occurrence  is 
2 a.m.,  when  it  wakes  from  sleep  and  lingers  for  an  hour  or 
two  unless  assuaged  by  food,  a warm  drink,  or  medicine. 
It  is  aggravated  by  lasting,  worry,  fatigue,  and  cold,  and 
sometimes  by  smoking.  It  is  relieved  by  food,  drink, 
warmth,  rest,  peace  of  mind,  and  alkalis.  Delayed  pain, 
first  noted  in  1828  by  Abercrombie  [11],  and  the  hunger- 
pain  with  relief  by  food  so  clearly  portrayed  by  Moynihnn 
(although  they  are  occasionally  due  to  other  causes — i.e. 
gall-stones,  appendicitis,  gastric  ulcer,  worry,  tobacco- 
excess,  and  very  rarely  carcinoma  of  the  stomach)  are  thus 
the  outstanding  features  of  the  disease. 

We  must  not,  however,  neglect  associated  symptoms. 
With  or  without  the  pain  an  epigastric  ‘sinking  sensation*, 
which  probably  represents  an  exaggeration  of  the  normal 
gastric  phenomena  of  hunger,  is  often  mentioned.  It  is  rare 
in  other  dyspepsias.  Feelings  of  ‘ flatulence’  or  of  fullness  or 
a ‘bursting  sensation’  may  accompany  or  replace  the  pain. 
In  nil  cases  of  dyspepsia  with  pronounced  flatulence  the  time 
of  arrival  of  the  symptom  should  be  determined.  If  this  is 
before  meals  and  food  gives  ease,  the  possibility  of  duodenal 
ulcer  (even  in  the  absence  of  pain)  must  be  seriously  con- 
sidered. The  relief  by  eructation,  and  especially  that  which 
follows  the  use  of  bicarbonate  of  soda,  suggests  to  the  patient, 
and  often  to  his  doctor,  that  the  case  is  ‘merely  one  of  flatu- 
lent dyspepsia’,  but  flatulent  dyspepsia  must  have  a cause, 
and  when  the  flatulence  is  rhythmical  and  at  its  worst  be- 
fore meals  this  cause  is  often  duodenal  ulcer.  The  gas  eruc- 
tated is  odourless  except  in  the  presence  of  pyloric  stenosis 
when  it  may  have  the  taint  of  sulphuretted  hydrogen. 
Vomiting  has  been  regarded  as  a rare  symptom  in  duo- 
denal ulcer  without  stenosis,  but  this  requires  qualification. 


100  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER 
Vomiting  of  food  is,  indeed,  exceptional,  but  on  acid  watery 
vomit  is  common  especially  with  the  more  chronic  ulcers. 
If  later  the  quantity  of  this  watery  vomit  increases  or  food 
is  mingled  with  it,  cicatricial  stenosis  should  be  suspected. 
Water-brash,  or  the  sudden  filling  of  the  mouth  with  taste- 
less watery  saliva,  sometimes  with  accompanying  pain  in 
the  parotid  glands,  is  common  and  so  characteristic  of  duo- 
denal ulcer  and  so  rare  in  other  dyspepsias  that  it  has 
genuine  diagnostic  value.  One  patient  spontaneously  and 
aptly  described  this  symptom  to  me  as  ‘a  beautiful  action 
of  Nature*.  Waking,  he  said,  at  night  with  bad  pain  he 
would  shortly  find  his  mouth  filling  with  water  as  fast  as  he 
could  swallow  it;  as  he  did  so  the  pain  steadily  faded  away. 
Heartburn  and  nausea  arc  not  symptomatic  of  duodenal 
ulcer.  Constipation,  especially  during  the  attacks,  is  a fre- 
quent complaint. 

Apart  from  the  local  symptoms  of  the  disease  there  arc 
certain  general  complaints  which  arc  very  real  to  the  patient 
and  sufficiently  rare  in  other  gastric  disorders  to  be  of  defini 
five  value.  I would  particularly  mention  a feeling  of  physi- 
cal weakness  or  exhaustion  which  is  coincidental  with  the 
pain  and  akin  to  feelings  experienced  in  association  with 
rectal  spasm,  excessive  purgation,  or  other  strong  visceral 
crises.  Mental  irritability  and  loss  of  the  power  of  concen- 
tration are  also  described  and  arc  evidence  of  the  power- 
ful nervous  influences  attendant  on  a visceral  disturbance 
which  carries  with  it,  as  well  as  pain,  the  psychic  and  physical 
phenomena  of  strong  hunger.  These  symptoms  also  are 
relieved  by  food. 

Factors  which  influence  Severity,  Character,  Situation,  or 
Food  Relationships  of  the  Pain 
It  should  be  mentioned,  for  it  is  not  as  widely  appreciated 
as  it  might  be,  that  the  degrees  of  physical  disturbance  in 
duodenal  ulcer  show  wide  variations.  The  physician  secs 
many  cases  in  which  the  very  mildness  of  the  symptoms  has 
led  to  a postponement  of  diagnosis.  The  suigeon,  no  doubt, 
sees  a higher  proportion  in  which  pain  is  outstanding  and 
severe.  The  severity  of  the  pain  tends  to  increase  with  the 


TIIE  NATURAL  HISTORY  OF  DUODENAL  ULCER  107 
chronicity  of  the  ulcer.  It  increases  at  first  with  com* 
mcncing  stenosis,  but  later,  as  gastric  dilatation  supervenes 
upon  hypertrophy,  pain  becomes  less  obtrusive  and  vomit- 
ing is  the  leading  symptom.  When  the  head  of  the  pan- 
creas is  eroded  by  a posterior  ulcer,  the  pain  is  at  times 
unbearably  severe  and  in  the  presence  of  this  complication 
I have  seen  courageous  men  reduced  to  exhaustion  and  tears. 
Apart  from  haemorrhage  it  is  the  only  symptom  which  the 
physician  may  he  called  upon  to  treat  with  morphine.  It  is 
worthy  of  note  that  haemorrhage  may  immediately  abolish 
pain.  When  bleeding  is  severe,  confinement  to  bed,  mor- 
phine, and  abstention  from  food,  and  later  a strict  dietary, 
clearly  explain  the  relief,  but  even  slight  and  at  first  un- 
recognized bleeding  in  an  ambulator}’  case  will  have  the 
same  effect.  In  this  circumstance  a patient  who  has  been 
suffering  dyspeptic  pains  may  actually  hold  himself  better 
as  regards  his  ulcer,  and  a failure  to  appreciate  the  signifi- 
cance of  developing  weakness  and  anaemia  results.  In  the 
presence  of  early  stenosis  pain  may  become  more  ‘grinding' 
or  ‘peristaltic’  in  quality.  The  situation  of  the  pain  com- 
monly shifts  to  the  right  in  the  case  of  old-standing  and 
adherent  ulcers.  The  interval  between  food  and  pain  dimin- 
ishes in  the  early  stages  of  pyloric  stenosis  and  may  be 
reduced  to  one  or  one  and  a half  instead  of  the  two  or 
three  hours  previously  experienced.  It  should  also,  however, 
be  recognized  that  patients  with  extreme  gastric  ‘hurry’ 
occasionally  show  a very  short  food-pain  interval.  With 
ulceration  involving  the  head  of  the  pancreas  all  clear 
relationship  to  food  tends  to  disappear  and  alkalis  may 
cease  to  be  effective. 


Objective  Signs 

In  the  absence  of  pyloric  stenosis  with  gastric  dilatation 
or  the  rare  discovery  of  a palpable  inflammatory  tumour  it  is 
too  widely  assumed  that  duodenal  ulcer  is  a disease  without 
physical  signs.  If  carefully  sought  for,  superficial,  or  more 
commonly  deep  cutaneous  soreness,  an  increased  abdomi- 
nal reflex,  muscular  guarding,  and  deep  tenderness — all 
confined  to  llic  right  upper  quadrant  of  the  abdomen — will 


108  TIIE  NATURAL  HISTORY  OP  DUODENAL  ULCER 
be  found  either  singly  or  in  various  combination  in  a high 
proportion  of  cases.  These  signs  are  more  likely  to  be  found 
with  anterior  ulcere,  during  stages  of  activity,  and  when 
pain  is  actually  present.  They  disappear  with  healing.  An 
increased  reflex  and  muscular  guarding  are  both  more  com- 
mon than  cutaneous  hyperalgesia.  Very  occasionally  a pilo- 
motor reflex  (goose-skin)  confined  to  the  same  area  may  be 
observed  when  eliciting  the  abdominal  reflex.  The  vaso- 
motor consequences  of  active  pain  are  sometimes  manifest 
in  the  facies.  Thus  near  relatives  describe  pallor  or  ‘grey- 
ness'  coincident  with  suffering  in  chronic  cases.  Phospha- 
turia  is  so  common  in  association  with  active  duodenal  ulcer 
that  I have  come  to  expect  a milky  urine  at  the  time  of 
consultation  in  the  majority  of  cases.  How  far  it  is  related 
to  the  taking  of  alkalis  or  not  I have  been  unable  to  deter- 
mine. Loss  of  weight  is  seldom  conspicuous  in  uncompli- 
cated cases. 


Complications  and  Sequelae 

Haemorrhage  and  perforation,  cicatricial  stenosis  and 
anchorage  of  the  ulcer-base  to  the  head  of  the  pancreas  are 
the  important  complications.  To  these  we  must  add  the 
unsuccessful  gastro-jejunostomy  which,  under  modem  con- 
ditions, has  been  a sufficiently  frequent  sequel  to  justify  its 
inclusion  in  a study  of  the  natural  history  of  duodenal  ulcer, 
and,  in  a retrospective  way,  may  even  help  to  illuminate 
the  disease. 

With  the  symptoms  of  haemorrhage  and  perforation  I 
shall  not  especially  concern  myself,  for  they  are  well  known. 
Haemorrhage,  as  stated,  occurs  in  about  one-quarter  of  the 
recognized  cases.  In  many  of  my  cases  there  was  a history 
of  two  or  more  haemorrhages;  107  patients  (series  a and  b ) 
between  them  had  151  haemorrhages.  Two  patients,  aged 
70  and  50,  died  of  gastric  uraemia  (alkalosis)  with  coincident 
haemorrhage,  in  1 case  following  an  operation.  One,  aged 
56,  died  of  coincident  haemorrhage  and  cellulitis  of  the  arm. 
One,  aged  36,  was  transfused  on  account  of  a severe  haemor- 
rhage from  a chronic  ulcer,  had  an  immediate  reaction, 
and  succumbed.  Three  cases,  aged  76,  72,  and  20,  died  of 


rjnoq  pfpojJid  iuojj  ticj.C  Anna  aoj  pajajjns  ‘cl  poSo  ‘jJn,l<ys  Pl°  anU  « 
'■y  Jofrp;  ‘tvtMuxxt  J'fl  futtpkwt  x/Jjn  jeujponp  jout/twl  fa  itvi  y 

•titcd  jo  osmro  oqq  5uun.\o3stp  oq  a\oia  u qquv  40 
4oojn  utr  ja  jotpj  oqq  joj  iMjprpapurt  strotjcjodo  qt?  uorpopp 
poduoso  pt?q  J3o;n  jcuoponp  quojoijpc  jouoqsod  v tpnpt 
ui  sosco  woos  ospi  oAttij  j *43t|q38oq|u  umuoponp  3ip  JO  J4cd 
qs4tj  oqq  sojtiDsqo  os  puu  'XqtAtqotr  otqprqsuDd  Saanp  qqStj 
oqq  oq  jdao  qstuqq  st  uttuquo  ouoj.'CdajcI  oqq  ‘uimraponp  oqq 
jo  tioiquxtj  tuitj  qqm  ‘asnuooq  ‘oAOtpq  j ‘Xiqjcd  ‘sosuo  osoqq 
ut  sq«.i3o[Oipcj  qtodxo  Xq  passuu  Xipiuotsoooo  st  stsouSmp 
oqj,  •siuoqduiXs  joo | n oqq  qqiAt  o2  pm?  omoo  qt  uoos  OAuq 
j pun  'sosuo  oiuos  tit  sanoDo  uunsooXij)  *posou3cjp  Xl3tIOJA\ 
souitqouios  ojoj340tjq  34U  snjnopjo  p?u34  putt  Xitij|t£i  ‘Xjxouaq 
-sod  qpj  Xpoup  oq  Xuui  pun  tno[  qqStJ  oqq  oq  q3noiqq 
pojjojoi  putt  qttujpcnb  joddn  qq3tj  oqq  ut  Xpiouiuioo  st  tired 
ot|X  ‘PH3*  SH  *oj  ouiqdiotu  Suumboj  uoao  pttu  ‘sqtrqic  pun 
qtrouquojq  jeotpottr  qouqsaq  Sutpuodsojqatr  ‘/qtJOAOspmsntm 
jo  uwd  Xq  pozuoqoujsqo  st  ipttpv  sdojoAop  otuoJpuXs  pomip 
uqtmosiqq  uj  *qt  opow  Xqunqon  Xout  40  ucSjo  stqq  oq  poppAV 
Xjuutj  oJout  outoooq  Xout  43Djn  oqq  jo  osuq  oqq  joqumu 
qums  u tij  *400[n  JotiaqsocT  jo  sosuo  Xuutu  ut  suotsoqpn 
Xq  suojoucd  oqq  oq  pojoqouu  ssofqqnop  st  uintioponp  oqx 
SV3U3UVJ  3t/j  fo  ju3tu3ap.au/ 

•SS3[  40  S4C3X  0A1J  JO  SOUOqsttJ 

oau3  so sco  c Xjuo  *S4UoX  uooquoAOs  scav  stsouoqs  ouopCd  jo 
sosuo  Xui  jo  01  ut  suioqdurXs  joopt  jo  uotqturtp  oScioac  dijx 


112  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER 
of  dyspepsia  with  pain  arriving  some  hours  after  food  and  relieved 
by  it.  Later  the  pain  became  greatly  intensified  and  less  clearly 
related  to  meals.  He  saw  a surgeon  who  diagnosed  gall-stones  and, 
in  spite  of  a negative  cholecystography,  operated  for  gall-stones. 
Finding  no  stones  he  drained  the  gall-hladdcr.  During  convalescence 
there  was  melacna  on  two  occasions.  The  pain  continued  as  before, 
and  in  his  worst  attacks,  which  took  place  at  night,  was  sometimes 
so  severe  as  to  make  him  weep;  it  was  accompanied  by  involuntary 
tremors  and  shivering.  I saw  him  in  pain  and  it  was  a pitiful  spec- 
tacle. The  pain  was  referred  to  the  level  of  the  eleventh  and  twelfth 
ribs  on  the  right  side  posteriorly  and  there  was  guarding  with  tender- 
ness over  the  right  upper  rectus.  I diagnosed  'posterior  duodenal 
ulcer  involving  the  pancreas’.  The  radiologist  reported  ‘appearances 
strongly  indicative  of  an  ulcer  of  the  stomach  about  half-way  between 
the  cardia  and  the  pylorus'.  Mr.  L.  Bromley  operated  and  found  no 
gastric  lesion  hut  a posterior  duodenal  ulcer  flnuly  welded  to  the 
head  of  the  pancreas.  A gastro-jejunostomy  was  performed  and  all 
symptoms  were  completely  relieved. 

Anastomotic  Ulcer 

For  every  10  cases  of  duodenal  ulcer  referred  to  me  I see 
one  case  of  anastomotic  ulcer.  This  gives  no  indication  of 
the  frequency  of  this  sequel,  for  it  is  evident  that  surgical 
‘failures’  find  their  way  to  the  physician  just  as  medical 
‘ failures  ’ find  their  way  to  the  surgeon.  The  sequel,  however, 
is  a serious  one  and  sufficiently  common  to  justify  careful 
inquiry  into  its  causes  and  the  greatest  caution  in  the  selec- 
tion of  cases  for  a gastro-jejunostomy. 

The  development  of  ulceration  at  or  near  the  stoma  has 
been  variously  attributed  to  faulty  technique,  unabsorbable 
sutures,  the  failure  to  eradicate  focal  sepsis,  and  neglect  of 
appropriate  after-care.  Jly  own  experience  suggests  that 
more  important  than  any  of  these  are  a faulty  judgement  in 
the  selection  of  cases  for  operation  and  the  presence  of  a 
strong  constitutional  predisposition.  There  was  a positive 
family  history  in  7 out  of  my  35  cases  of  anastomotic  ulcer 
(6),  twice  the  rate  of  incidence  in  the  duodenal  ulcer  series 
(a).  The  age  at  onset  of  the  ulcer-symptoms  for  which  the 
operation  was  undertaken  was  under  20  years  in  0 cases 
and  in  3 of  these  there  was  a positive  family  history.  Early 
appearance  of  a chronic  disease  more  usual  in  later  decades 
should  always  suggest  constitutional  predisposition.  I have 


114  THE  NATURAL  HISTORY  OF  DUODENAL  ULCER 
those  of  the  original  duodenal  ulcer.  There  is  hunger-pain 
with  more  or  less  relief  by  food.  Both  immediate  and  lasting 
relief  of  symptoms,  however,  even  with  the  strictest  medical 
care,  is  much  less  certainly  attained  than  in  the  case  of 
duodenal  ulcer.  Furthermore,  pain  and  distress  tend  to  be 
more  severe  and  lasting.  Haemorrhage  may  occur  without 
premonitory  pain.  The  most  constant  physical  sign  is  a 
point  of  tenderness  just  above  and  to  the  left  of  the  navel. 
Anastomotic  ulcers  are  liable  to  the  same  leading  complica- 
tions os  duodenal  ulcer — namely,  haemorrhage,  perforation, 
and  stenosis.  The  most  wretched  and  often  fatal  complica- 
tion is  a gastro-jejuno-colic  fistula  of  which  the  symptoms 
are  pain,  eructation  of  ‘bowel-wind’,  or  even  vomiting  of 
faeces,  diarrhoea,  anaemia,  and  emaciation.  Fortunately  it 
is  rare.  I have  had  two  cases  under  my  care  in  hospital  and 
one  in  private  practice.  Hamilton  Fairley  and  Kilner  have 
recently  reported  on  cases  showing  fatty  diarrhoea  with  a 
megnlocytic  anaemia  [12]. 

Other  Complications  of  the  Short  Circuit 

The  most  important  remaining  complication  is  ‘vicious 
cycle  vomiting ’,  which  is  characterized  by  attacks  of  copious 
bilious  vomiting  at  irregular  intervals  with  or  without  pain. 
The  ‘dumping  stoma’,  in  which  the  common  complaint  is 
of  n fullness  and  discomfort  around  and  below  the  navel 
developing  soon  after  meals  and  due  to  rapid  over-filling  of 
the  small  gut,  is  inconvenient  but  less  crippling. 

The  Prospects  of  other  Operations  and  Medical  Treatment 

It  is  too  early  to  assess  the  later  results  of  alternative 
operations  such  as  gastro-duodenostomy,  resection,  and 
excision.  Only  after  some  twenty  years  are  we  learning  to 
view  in  correct  perspective  the  advantages  and  disadvan- 
tages of  gasfro-jejunostomy,  and  if  we  are  wise  we  shail  not 
too  trustfully  accept  the  promises  made  on  behalf  of  the 
newer  experiments.  That  they  do  not  always  succeed  is 
already  apparent.  That  they  will  often  fail  in  the  presence 
of  strong  constitutional  predisposition  or  with  injudicious 
selection  of  cases  seems  to  me  probable.  Medical  treatment 


11C  THE  NATURAL  IIISTORY  OF  DUODENAL  ULCER 
likelihood  of  perforation  by  increased  intraduodenal  pressure 
(as  I have  once  successfully  foretold)  [18].  My  policy  is  to 
oppose  surgical  treatment  in  youthful  cases ; in  non-obstruc- 
tive cases  with  short  histories  and  adverse  pedigrees  or  not 
previously  accorded  a strict  medical  treatment;  in  cases 
with  recent  haemorrhage,  lacking  other  indications;  and  in 
cases  in  which  X-ray  and  test-meal  show  gastric  ‘ hurry  for 
here  to  accelerate  emptying  still  further  and  to  attempt  an 
anastomosis  in  the  presence  of  exaggerated  motor  and  chemi- 
cal unrest  is  to  create  just  those  conditions  which  may  be  he]  d 
to  favour  secondary  ulceration.  Highly  nervous  individuals 
and  elderly  subjects  should  often  be  deemed  unsuitable 
for  surgery,  even  when  the  only  alternative  is  continuous 
medical  and  dietary  care.  Economic  and  environmental 
factors  must  at  times  compel  a modification  of  general 
policy.  Surgical  treatment  should  always  be  followed  by 
a period  of  strict  medical  treatment  and  proper  precautions 
thereafter.  Psychological  as  well  as  physical  requirements 
must  be  carefully  studied. 

All  surgeons  and  physicians  who  undertake  the  treatment 
of  this  troublesome  disease  must  endeavour  to  preserve  the 
studious  attitude,  not  lightly  accepting  opinion  or  submit- 
ting to  the  bias  of  their  craft,  and  remembering  always  that 
they  are  not,  in  fact,  concerned  with  duodenal  ulcer  the 
lesion,  but  with  duodenal  ulcer  the  disease,  as  it  occurs  and  as 
it  varies  in  individuals  of  special  type  and  temper  and  differ- 
ing daily  circumstance.  In  each  case,  briefly,  judgement 
must  be  based,  not  upon  the  presence  of  an  ulcer,  but  upon 
a proper  understanding  of  the  whole  patient  and  the  whole 
disease. 

As  I have  sought  to  show,  duodenal  ulcer  has  general 
effects  on  the  body  and  the  mind  as  well  as  general  causes 
in  them,  and  no  effect  or  cause  can  be  neglected. 

In  a restless  and  fretful  age  which  has  largely  lost  the  old 
simplicities  of  diet  and  conduct,  the  most  important  contri- 
bution which  we  can  make  to  the  prophylaxis  of  duodenal 
ulcer  is  to  furnish,  as  opportunity  arises,  sensible  instruc- 
tions to  the  community  (and  particularly  to  such  families 
or  individuals  as  manifest  a constitutional  or  occupational 


THE  NATURAL  HISTORY  OF  DUODENAL  ULCER  117 
predisposition  to  the  disease)  with  regard  to  the  evils  of 
missed  and  bolted  meals,  of  excessive  smoking,  and  of  the 
prevalent  habit  of  attempting  to  combine  the  process  of 
digestion  with  anxiety  and  affairs.  It  is  not  extravagant  to 
suppose  that  a cup  of  hot  milk  at  11  a.m.  and  bedtime 
would  save  many  a harassed  doctor  or  business  man  endowed 
with  the  diathesis  from  developing  the  disease. 

The  most  important  contribution  which  wc  can  make  to 
the  therapeutics  of  duodenal  ulcer  is,  by  observing  subjec- 
tive symptoms,  to  ensure  much  earlier  diagnosis,  and,  by 
observing  the  entire  disease  and  the  qualities  of  its  victims, 
to  achieve  a wiser  balance  in  our  choice  of  method. 

It  is,  I believe,  a just  criticism  of  surgery  and  medicine  in 
the  present  era  that  they  have  concentrated  on  parts  to  the 
exclusion  of  the  whole  and  on  technique  to  the  exclusion  of 
philosophy.  In  duodenal  ulcer  no  less  than  in  many  other 
maladies,  wc  have  come  to  rely  upon  too  narrow  a patho- 
logy. In  our  therapeutic  quests  wc  have  been  too  little 
observant  of  physiological  principle.  Wc  are  nil  compelled 
by  the  magnitude  of  our  subject  to  be  somethingof  special- 
ists, but  this  should  not  necessitate  an  abandonment  of  that 
naturalistic  outlook  which  marked  the  achievement  of  our 
old  preceptors  from  Hippocrates  to  Hunter. 

REFERENCES 

1.  Wilkie,  D.  I*.  D.:  Lancet,  1927,  li.  1228. 

2.  Nielsen,  N.  A.:  Ada  Med.  Scand.,  1923,  Iviil.  1. 

3.  Faber,  K.;  Arch,  des  Malad.  de  VAppar.  Digest.,  1920,  xvl,  909. 

4.  Moody,  K.  O.,  Van  Nuys,  R.  G.,  and  Chamberlain,  IV.  E.j 

Joum.  Amer.  Med.  Assoc.,  1923,  lxxxi.  1921. 

5.  Campbell,  J.  M.  II.,  and  Conybeare,  J.  J.:  Guy's  tlosp.  Hep., 

1921,  lxxiv.  351. 

0.  Bennett,  T.  I.,  and  Ryle,  J.  A.:  Ibid.,  1921,  Ixxl.  280. 

7.  Hurst,  A.  F.s  Ibid.,  450. 

8.  and  Stewart,  M.  J.z  Gastric  and  Duodenal  Ulcer.  London, 

1029. 

0.  Moyntitan,  Lord:  Brit.  Med.  Joum.,  1932,  i.  1. 

10.  Duodenal  Ulcer.  London,  1012. 

31.  Abercrombie,  J.:  Pathological  and  Practical  llesearehes  on 

Diseases  of  the  Stomach,  Are.,  3rd  edition.  London,  1837. 

12.  Pair  ley,  N.  H.,  und  Kilner,  I'.  T.:  Lancet.  1931,  II.  1335. 

13.  Ryle,  J.  A.:  Gup's  Itosp.  Jlcp.,  1020,  Ixxvi.  102. 


ANOREXIA1 


Few  expressions  of  physical  and  mental  well-being  are 
more  widely  accepted  and  more  generally  opprecinted  than 
a good  appetite-  Conversely,  few  subjective  symptoms, 
apart  from  actual  pain,  more  promptly  perturb  the  indivi- 
dual and  attract  the  comment  of  bis  friends  than  failure  of 
appetite.  In  trying  to  assess  the  progress  of  sick  persons, 
the  continued  suppression  or  the  return  of  the  desire  for 
food  are  indices  upon  which  we  place  daily  reliance.  In  our 
own  personal  experiences  of  ill  health  we  recognize  with 
each  trivial  febrile  ailment  that  an  abolition  of  our  interest 
in  meals  constitutes  a part  of  the  malaise,  and  even  in  those 
lesser  states  of  impaired  fitness  which  we  ascribe  to  periods 
of  overwork  or  to  some  access  of  fatigues  and  worries,  a 
diminished  enjoyment  of  food  is  familiar. 

We  thus  observe  all  gradations  of  anorexia,  or  ‘the  loss 
of  the  desire  for  food \ Its  slightest  forms  are  represented 
by  those  minor  shades  of  disinclination  just  mentioned.  At 
the  opposite  end  of  the  scale  is  anorexia  in  its  gravest  degree 
occurring  as  a symptom  of  many  chronic  diseases  and  accom- 
panying the  active  phases  of  acute  fevers.  In  illness  of 
intermediate  severity  every  intermediate  grade  of  anorexia 
may  be  encountered.  It  would  therefore  seem  that  appetite 
is  an  important  and  even  a delicate  physical  response,  and 
that  wc  should  have  some  understanding  of  its  mechanism. 

Appetite  is  so  essentially  a manifestation  of  normal  bodily 
health  that  we  should  expect  the  physiologist  to  provide 
us  with  valuable  information  concerning  it.  I hope  to  show 
you  that  the  clinical  study  of  anorexia  may  also  help  to 
illuminate  the  problem  for  the  physiologist. 

What  do  we  understand  by  appetite,  and  how  far  is  it 
identical  with  or  different  from  hunger?  It  is  best  charac- 
terized, I think,  as  a desire  or  readiness  for  food,  and  it  is 
customarily  regarded  as  a pleasant  sensation.  Hunger,  on 
1 Guy' a Hasp . Gcatile,  1024,  xxxviii.  305. 


120  ANOREXIA 

Pleasant  tastes,  pleasant  aromas,  a table  well  arranged,  the 
dinner-bell,  or  the  clink  of  spoons  or  glasses,  and  even  the 
tactile  sensory  comforts  of  evening  dress  and  clean  napery, 
have  all  become  inextricably  associated  with  the  idea  of 
food,  and  singly  or  together  are  capable  of  promoting  or 
enhancing  appetite. 

Camion  [3]  says:  ‘Appetite  is  related  to  previous  sensa- 
tions of  the  taste  and  smell  of  food.  Sensory  associations, 
delightful  or  disgusting,  determine  the  appetite  for  any 
edible  substance,  and  either  memory  or  present  stimula- 
tion can  arouse  the  desire.’  And  yet  it  must,  I believe,  be 
concluded  that  these  memories  in  turn  evoke  some  local 
response.  We  know  from  Pavlov’s  experiments  that  a local 
secretory  response  to  the  more  direct  appetite  stimuli  does 
occur,  and  it  is  not  improbable  that  similar  physical  re- 
sponses may  be  evoked  by  food-memories. 

While  contending  that  appetite  is  a complex  and  largely 
psychic  phenomenon,  modem  observers  have  claimed  a 
much  more  special  character  for  the  sensation  of  hunger, 
which  Cannon  and  Washbumc  [3]  and  Carlson  [4]  have 
shown  by  the  most  careful  experiments  to  be  associated  with 
and  actually  due  to  peristaltic  contractions  of  the  stomach. 
These  they  ‘graphically  recorded  with  the  aid  of  rubber 
balloons  and  correlated  with  the  hunger  sensations.  They 
admit,  of  course,  that  other  sensations  such  as  faintness  and 
weakness  may  accompany  prolonged  hunger,  but  regard  the 
actual  hunger-discomfort  as  a gastric  phenomenon.  Is  there 
any  good  evidence  that  appetite  has  also  a local  manifes- 
tation or  a local  cause  ? When  asked  to  describe  and  locate 
the  sensation  of  appetite  people  will  provide  the  most 
variable  answers,  but  there  is  a general  tendency  to  refer 
it  to  the  pharynx,  the  oesophagus,  or  the  epigastric  zone, 
and  this  reference  seems  to  me  to  indicate  that,  as  in  hunger 
or  the  craving  for  food,  so  in  appetite  or  the  readiness 
for  food  there  is  a local  process  concerned.  Subjective 
experience  and  clinical  observation  suggest  that  the  local 
process  may  be  associated  with  the  tonic  activity  of  the 
upper  alimentary’  tract,  much  as  hunger  is  associated  with 
peristaltic  activity;  and  that  just  as  general  well-being  and 


ANOREXIA  121 

preparedness  for  physical  effort  are  associated  in  idea  and 
fact  with  a favourable  state  of  tonus  and  adaptability  in  the 
skeletal  muscles,  so,  too,  digestive  well-being  and  prepared- 
ness for  gastric  effort  arc  associated  with  a favourable  state 
of  what  might  be  termed  ‘anticipatory  tonus*  in  the  gastric 
musculature.  Moreover,  there  is  an  undoubted  association 
between  the  two  states — that  of  general  physical  well-being 
and  that  of  local  digestive  well-being.  Wc  know  that  nothing 
is  more  conducive  to  a good  appetite  than  a healthy  open- 
air  holiday  with  plenty  of  exercise,  or  the  procedure  of 
training  for  an  athletic  contest. 

In  support  of  the  view  that  appetite  is  partly  a local 
process  connected  with  visceral  tonus,  wc  have  also  clinical 
and  radiographic  observations  of  gastric  function  in  certain 
general  and  gastric  diseases  associated  with  a poor  or  absent 
appetite.  In  conditions  such  as  the  debility  due  to  prolonged 
fevers  or  accompanying  tuberculosis  and  visceroptosis 
gastric  hypotonus  is  a frequent  finding.  In  gastric  carcino- 
mata which  so  infiltrate  the  wall  of  the  stomach  as  to 
render  it  incapable  of  normal  tonic  and  peristaltic  activity, 
anorexia  is  present  almost  more  constantly  and  in  more 
pronounced  degree  than  in  any  other  malady,  and  as  a 
symptom  of  the  disease  itself  is  as  constant  as  pain. 

This  fact,  that  the  most  complete  loss  of  appetite  occurs 
in  some  diseases  in  which  there  is  no  impairment  of  the 
mental  faculties  and  no  interference  with  the  special  senses, 
is  an  argument  in  favour  of  the  local  appreciation  of  appetite 
being  dependent  on  a local  phenomenon. 

If  we  wished  experimentally  to  show  a relationship 
between  gastric  tonus  and  the  sensation  of  appetite,  wc 
should  have  to  evolve  a method  of  rendering  tire  wall  of 
the  stomach  rigid  and  incapable  of  tonic  contraction  and 
adaptation,  without  modifying  the  other  functions  of  the 
body,  without  producing  fever  or  the  cachexia  of  malig- 
nant disease,  and  without  inducing  the  debility  v.  hich  arises 
from  pain  or  other  physical  or  mental  discomforts.  Very 
occasionally  Xnturc  performs  this  experiment  for  us  by 
means  of  the  disease  which  lias  been  variously  described  as 
Uuitis  plastica,  leather-bottle  stomach,  and  cirrhosis  of  the 


122  ANOREXIA 

stomach.  This  condition  is  now  regarded  as  cancerous,  but 
in  a small  proportion  of  cases  it  seems  that  patients  may 
live  for  months  or  even  for  years  without  the  development  of 
any  severe  pain,  and  without  grave  cachexia  or  dissemina- 
tion of  metastases.  Profound  loss  of  appetite  may,  however, 
be  present. 

I have  seen  one  such  case.  A man  in  the  forties  had  com- 
plained for  two  years  of  complete  loss  of  appetite.  He  was 
leading  throughout  this  period  a most  active  life,  both 
physically  and  mentally ; he  played  games  with  vigour,  but 
no  measures  which  he  could  adopt  and  no  treatment  pre- 
scribed produced  the  slightest  amelioration  of  his  symptom. 
He  did  not  experience  pain,  and  his  loss  of  weight  was  not 
more  than  would  be  accounted  for  by  his  diminished  intake 
of  food.  On  clinical  and  radiographic  evidence  a diagnosis 
of  leather-bottle  stomach  was  suggested,  and  was  later 
confirmed  at  operation.  As  there  is  often  no  obstruction  at 
any  point,  pain  need  not  necessarily  be  a symptom  in  these 
cases,  but  hunger,  which  depends  on  peristaltic  activity  and 
appetite,  which  I believe  to  be  in  part  an  expression  of  gas- 
tric tonus,  must  both  be  inhibited. 

Other  conditions  in  which  there  is  local  damage  to  the 
stomach-wall  with  loss  of  appetite  include  pyloric  stenosis 
when  the  stage  of  atonic  dilatation  has  been  reached,  and 
alchoholic  gastritis.  In  the  former,  tonus  is  obviously  im- 
paired. In  the  latter,  although  secretion  and  motility  are 
deranged  and  the  mouths  of  the  gastric  glands  are  blocked 
with  mucus,  the  whole  economy  has  been  so  much  influenced 
by  the  prolonged  poisoning  that  it  would  not  be  fair  to 
assume  that  the  anorexia  was  a direct  expression  of  the 
local  disease  alone. 

Have  secretory  abnormalities  any  influence  on  the  sensa- 
tion of  appetite?  There  is,  as  a matter  of  fact,  little  evi- 
dence that  the  secretory  behaviour  of  the  stomach  per  sc 
in  any  way  modifies  its  sensations.  Free  HC1  may  be 
present  in  excess  of  the  average  or  absent  altogether  in  both 
healthy  and  unhealthy  individuals  without  any  gastric 
discomfort,  and  without  appreciable  modifications  of  hunger 
or  appetite.  Undoubtedly  there  is  often  a scanty,  or  even 


ANOREXIA  123 

an  absent,  secretion  vr hen  anorexia  is  present,  as,  for  instance, 
in  cancer  and  gastritis,  but  we  have  better  reasons  for 
incriminating  the  impaired  tonus  and  motility  than  the 
diminished  secretion.  Beaumont  [1]  showed  that  a very 
inflamed  condition  of  the  gastric  mucosa  with  almost  com- 
plete suppression  of  secretion  might  follow  on  alcoholic  bout 
in  the  case  of  Alexis  St.  Martin  without  the  production  of 
any  subjective  symptoms. 

Assuming  that  appetite  may  be  in  part  an  expression  of 
healthy  gastric  tonus,  and  that  it  is  at  least  a fair  statement 
to  say  that  impaired  tonus  and  impaired  appetite  occur 
together,  have  we  any  evidence  that  hypertonus  is  accom- 
panied by  increased  appetite?  In  many  cases  of  duodenal 
ulcer,  in  which  the  stomach  is  demonstrably  of  hypertonic 
type,  appetite  is  exaggerated,  although  for  fear  of  aggravat- 
ing their  pain  the  patients  inay  curtail  their  meals.  It  is 
also  stated  that  the  increased  appetite  and  hunger  of  dia- 
betes may  be  accompanied  by  the  radiographic  features  of 
gastric  hypertonus. 

Briefly  to  summarize  our  knowledge  in  regard  to  appetite, 
I think  we  may  say  that  tJie  sensation  is  in  part  a memory 
process  a)ui  in  part  a local  manifestation  of  efficient  alimentary 
tonus  reflcxly  induced  by  the  memory  stimulus,  or  by  the  more 
direct  stimuli  of  seeing , tasting,  or  smelling  food,  or  by  some 
combination  of  these  several  factors.  This  view  helps  to  ex- 
plain the  close  similarity  between  the  appetite  and  hunger 
sensations  as  well  as  their  essential  differences,  for  tonic 
and  peristaltic  activity  are  kindred  phenomena,  but  not 
synonymous. 

Let  us  next  consider  the  things  which  in  health  may 
modify  appetite.  Fresh  air,  exercise,  cold  weather,  and  a 
happy  mind  are  amongst  the  important  adjuvants,  all  being 
calculated  to  encourage  an  active  mul  well-balanced  meta- 
bolism. Conversely  an  indoor  sedentary  life  and  a heated 
atmosphere,  or  a worried  or  over-worked  mind,  arc  cal- 
culated to  impair  appetite,  aud  in  many  eases  actually  do 
produce  such  a loss  of  appetite  and  general  well-being  as  to 
amount  to  real  ill  health.  The  effect  of  certain  emotions  on 


124  ANOREXIA 

the  appetite  is  pronounced.  Falling  in  love,  or  a great 
bereavement,  or  a grave  domestic  or  business  anxiety,  may 
for  a time  determine  a real  anorexia.  Of  these  states,  how- 
ever, which  come  to  trouble  otherwise  sound  and  healthy 
mortals,  the  majority  are  temporary  and  recoverable.  The 
fatty  and  oily  foods  which  inhibit  appetite  and  may  even 
cause  nausea  can  be  shown  experimentally  to  be  inhibitors 
both  of  gastric  motility  and  secretion. 

In  reviewing  anorexia  as  a symptom  of  established  disease, 
some  classification  of  causes  becomes  desirable.  The  follow- 
ing is,  I think,  os  convenient  os  any: 

Causes  of  Anorexia 

1.  Acute  febrile  illnesses. 

2.  Chronic  infective  illnesses,  especially  tuberculosis. 

3.  Other  chronic  debilitating  diseases,  especially  malig- 
nant disease. 

4.  Local  disease  of  the  stomach,  especially  carcinoma  and 
chronic  gastritis. 

5.  Mental  and  emotional  derangements,  neurasthenic 
states,  nervous  dyspeptic  states,  and  ‘anorexia  ner- 
vosa*. 

Having  drawn  your  attention  to  the  frequency  of  lost 
appetite  as  a symptom  in  the  mild  as  well  as  the  graver 
types  of  disease,  it  might  appear  superfluous  to  compile 
such  a special  and  limited  list  of  causes.  My  reason  is  that 
in  the  types  of  disease  included  in  this  list,  anorexia  is  a 
symptom  of  special  importance  from  the  diagnostic  or 
prognostic  point  of  view.  In  some  instances,  again,  the 
treatment  of  the  symptom  itself  may  play  a part  in  modi- 
fying the  course  of  the  disease,  or  even  in  producing  a cure. 

In  the  acute  febrile  illnesses  there  is  a general  arrest  of 
many  normal  processes.  The  skeletal  muscles  become  weak 
and  flaccid;  the  secretions  of  the  salivary,  gastric,  and  other 
glands  are  diminished ; the  urinary  output  falls.  The  tissues 
are  given  over  to  measures  of  defence,  and  digestion  and 
assimilation,  except  of  water,  are  largely  in  abeyance.  It 
is  not  surprising  that  the  gastric  musculature,  like  the 
skeletal  musculature,  should  suffer  fatigue  and  loss  of  tone. 


ANOREXIA  125 

and  that  the  clouded  senses  should  cease  to  be  responsive 
to  the  stimulus  even  of  the  most  carefully  chosen  diets. 
Thirst  may  be  great,  but  the  lack  of  appetite  for  solid 
food  indicates  the  unreadiness  of  the  stomach  for  ordinary 
digestive  efforts.  The  moment,  however,  the  infection  is 
overcome  we  find  a change  in  the  sensations  and  inclinations 
of  the  patient.  Very  early  in  convalescence  from  pneumonia 
and  still  more  after  typhoid  fever,  the  appetite  improves 
and  may  even  become  voracious. 

In  chronic  insidious  infections  such  os  pulmonary  tuber- 
culosis, loss  of  appetite  may  be  of  diagnostic  as  well  as 
prognostic  value.  It  is  quite  frequently  an  early  symptom, 
and  when  we  find  a young  adult  with  a tendency  to  easy 
fatigue,  a waning  appetite,  a slight  loss  of  weight — without 
other  adequate  explanation — we  are  always  at  pains  to  ex- 
clude or  to  discover  n pulmonary  lesion.  In  the  more  active 
phases  of  the  disease  anorexia  is  a well-rccognizcd  symptom. 
Both  in  the  early  and  later  stages  there  is  a special  tendency 
to  loss  of  the  breakfast  appetite.  When  the  night  has  been 
disturbed  by  sweats  nnd  the  morning  by  cough  and  expec- 
toration this  is  readily  understandable;  it  is  not  quite  so 
easily  explained  in  the  incipient  or  the  scmi-quicsccnt  coses, 
but  I have  supposed  that  it  here  expresses  the  toxic-fatigue 
state  following  the  evening  auto-inoculation  of  the  previous 
day.  Those  who  work  in  sanatoria  arc  familiar  with  the 
sometimes  remarkable  increase  in  the  intake  of  food  which 
is  registered  in  those  cases  which  arc  ‘doing  well’  in  respect 
of  their  general  response  to  infection.  This  may  he  long 
before  the  physical  signs  point  to  appreciable  local  pro- 
gress. Improvement  of  appetite  goes  hand  in  hand  with 
stabilization  of  temperature  and  gaining  weight.  In  a 
disease  in  which  good  nourishment  is  so  vital  it  is  obviously 
of  the  first  importance  to  encourage  appetite  in  every  way, 
and  in  the  good  sanatorium  the  quality,  preparation,  and 
serving  of  the  food  arc  matters  for  special  attention.  In 
the  late  phases  of  disseminating  malignant  growth  loss  of 
opjictitc  is  almost  the  rule  wherever  the  primary  disease 
may  have  been,  but  the  alimentary  grow  tbs  are  more  apt 
to  promote  the  symptom.  In  carcinoma  vcntriculi  anorexia 


120  ANOREXIA 

is,  as  I have  mentioned,  a very  constant  symptom,  and 
according  to  Brinton  [5]  is  present  in  85  per  cent  of  cases. 
It  may  develop  quite  early  (one  patient  told  me  that  his 
earliest  symptom  was  loss  of  appetite  for  bread),  and  I am 
inclined  to  think  its  degree  bears  a definite  relation  to  the 
extent  of  stomach-wall  involved.  In  every  dyspepsia,  but 
especially  those  which  originate  during  or  after  middle  life, 
inquire  particularly  about  the  appetite.  This  may  occa- 
sionally help  to  differentiate  growth  from  chronic  ulcer. 
Generally  in  duodenal  ulcer  the  appetite  is  good;  in  large 
lesser  curvature  ulcers  and  the  mechanical  obstructions 
resulting  from  scarring  the  appetite  may  become  impaired ; 
but  it  is  rare  in  any  of  these  conditions  to  meet  with  the 
complete  abolition  of  appetite  or  positive  aversion  to  food 
peculiar  to  gastric  cancer. 

In  chronic  alcoholism  poor  appetite  is  again  familiar.  It 
is  most  noticeable  in  the  morning,  and  in  bad  cases  may 
be  associated  with  the  equally  familiar  morning  nausea, 
retching,  and  vomiting.  When  abstinence  is  observed  and 
the  gastritis  is  treated  by  lavage  or  other  suitable  measures 
there  is  a rapid  recovery  of  appetite. 

Some  degree  of  anorexia  is  common  in  neurasthenia.  By 
neurasthenia  we  should  properly  understand  a condition  of 
nervous  exhaustion  consequent  upon  physical  or  mental 
fatigue,  fear,  operations  or  illnesses  or  anxieties,  or  upon 
combinations  of  these.  Having  regard  for  the  general  loss 
of  vitality  and  * tone’  in  these  cases,  the  symptom  is  one 
which  we  should  expect.  It  may  be  an  important  one 
to  treat,  for  the  vicious  circle  of  fatigue,  loss  of  appetite, 
under-nutrition,  and  consequently  more  fatigue,  may  to 
some  extent  be  broken  by  careful  attention  to  the  dietary. 
Cold  beef  appearing  for  the  third  day  in  succession  may  even 
discourage  the  hunter  with  his  proverbial  appetite,  but  for 
the  limp  and  weary  neurasthenic  it  can  only  buttress  the 
misery  of  his  existence.  On  the  other  hand,  a dainty  repast 
of  small  and  well-cooked  viands  may  do  real  physical  good, 
and  help  to  restore  a little  of  the  joy  of  living,  or  at  least  the 
will  to  recover  it.  Needless  to  say  it  is  a small  part  of  the 
treatment,  but  in  a complaint  for  which  there  is  no  panacea 


ANOREXIA  I2T 

it  is  one  of  the  many  small  parts  which  we  cannot  afford  to 
neglect. 

Among  the  writings  of  Sir  William  Gull  [6],  there  arc  few 
more  interesting  than  that  which  deals  with  the  disease 
which  he  called  anorexia  nervosa.  We  arc  accustomed  to 
think  of  the  functional  nervous  diseases,  harassing  though 
they  often  are  both  to  their  victims  and  their  physicians,  ns 
seldom  actually  dangerous  to  life.  Here,  however,  is  one 
which  may  lead  to  death  from  starvation,  or  to  such  emaci- 
ation as  to  recall  the  cruellest  effects  of  war  conditions 
or  of  famine.  When  we  sec  our  first  advanced  case  of 
anorexia  nervosa  it  may  be  impossible  to  believe  that  the 
sufferer  has  no  underlying  physical  malady,  and  we  arc  very 
properly  anxious  to  discover  signs  of  tuberculosis,  diabetes, 
or  other  organic  wasting  disease.  The  subjects  arc  mostly 
young  women,  but  young  men  arc  not  immune.  There  may 
be  a personal  or  family  history  of  emotional  instability.  We 
find  that  there  has  been  for  some  time  general  failure  of 
appetite,  or  at  any  rate  a refusal  to  cat,  often  without  any 
other  striking  subjective  symptom.  Various  diagnoses  will 
probably  ulrcady  have  been  suggested,  and  at  the  present 
day  psycho-analytic  methods  may  have  been  employed, 
with  indifferent  success  or  even  with  aggravation  of  the 
trouble. 

The  physical  stigmata*  of  anorexia  nervosa,  opart  from 
the  pronounced  loss  of  weight,  include  an  overgrowth  of 
downy  hair  on  the  trunk  and  limbs,  constipation,  amcnor- 
rhoea,  and  a slow  ‘starvation*  pulse.  The  mental  stigmata 
include  moodiness,  resentment  of  maternal  solicitude,  and 
often  a restless  activity  of  mind  and  body  which  contrasts 
strangely  with  the  poor  physical  state.  Among  33  eases  in 
my  files,  35  were  females.  The  common  agc-incidcnce  is 
between  15  and  25  years;  Unhappy  kncattaics,  home 
disagreements,  and  voluntary  attempts  at  * slimming*  arc 
recognized  among  the  ‘causes’  of  the  disorder.  Two-thirds 
of  my  cases  were  psycho-neurotics  and  gave  no  clue  to 
suggest  that  the  beginnings  of  their  illness  were  physical. 
In  one  quarter  the  anorexia  appeared  to  develop  on  the 
basis  of  an  illness  or  an  operation*  The  remainder  were 


128  ANOREXIA 

psycliotics.  ltccovcry  at  home  is  rarely  possible,  but 
with  removal  to  suitable  surroundings,  close  supervision, 
and  insistence  on  an  adequate  food  intake,  many  of  these 
cases  may  be  restored  to  physical  and  mental  health.  In 
one  case,  seen  with  Sir  Arthur  Hurst,  radiography  showed 
the  stomach  to  be  peculiarly  large  and  atonic.  The  patient 
made  a complete  recovery.  It  was  judged  unwise  to  repeat 
any  investigations,  so  that  we  do  not  know  whether  gastric 
volume  and  tonus  became  normal  again.  It  is  not  im- 
probable that  the  local  appearances  in  the  first  instance 
were  evidence  of  a genuine  atony  induced  by  the  prolonged 
mental  and  nervous  depression  and  starvation. 

Sir  James  Goodhart  [7],  in  his  lectures  on  the  common 
neuroses,  suggests  that  the  term  ‘anorexia  nervosa*  might 
also  be  extended  to  those  much  more  numerous  sufferers 
from  nervous  types  of  dyspepsia.  These  patients  commonly 
complain  that  they  cannot  eat  this  and  they  cannot  eat 
that;  their  choice  of  foodstuffs  is  sometimes  peculiar  and 
irrational.  They  number  among  their  ranks  a host  of 
nervous,  voluble,  sparrow-likc  women  with  sparrows’  ap- 
petites. Personally  I should  prefer  to  keep  the  name 
‘anorexia  nervosa’  for  the  disease  more  clearly  defined  by 
Gull.  Say  that  these  others  have  a nervous  anorexia  if  you 
like,  but  they  seldom  show  signs  of  dying.  Far  from  it.  They 
will  hop  into  your  consulting-room  and  twitter  forth  their 
woes;  they  will  neither  gain  weight  nor  appreciably  lose  it; 
they  will  try  many  treatments  and  ask  for  more.  If  you  can, 
by  some  combination  of  severity  and  tact,  persuade  them  to 
cat  larger  amounts  of  more  ordinary  food  you  may  occa- 
sionally do  them  a real  service.  Their  dyspepsias  and 
anorexias  are,  I believe,  more  often  due  to  or  encouraged  by 
under-nutrition  than  by  any  of  the  supposedly  noxious  food- 
stuffs or  other  factors  which  they  themselves  incriminate. 
The  neurotic,  like  the  neurasthenic,  tends  to  eat  too  little, 
and,  as  he  or  she  is  commonly  caught  in  a circle  of  evils, 
many  of  them  hard  for  us  to  grasp,  it  is  a comfort  to  have 
one  point  at  which  a rational  attempt  may  be  made  to  break 
the  spell. 

In  the  very  young  we  encounter  yet  another  variety  of 


ANOREXIA  120 

functional  anorexia.  It  affects  the  nervous  children  of 
anxious-minded  parents,  and  is  often  largely  to  be  attri- 
buted to  the  reputation  for  poor  eating  which  the  parents 
have  repeatedly  given  them  and  conversed  about  in  their 
presence.  Being  more  plastic  than  adults  and  very  sug* 
gestible,  it  is  possible,  with  parental  co-operation,  to  get 
them  to  eat  well  again  by  a simple  process  of  judicious 
neglect,  combined  with  the  positive  assurance  afforded  by 
telling  others  in  their  presence  what  good  appetites  they 
have.  It  is  important,  however,  to  remember  that  loss  of 
appetite  in  children  (just  as  in  adults)  may  be  an  early 
symptom  of  physical  disease. 

REFERENCES 

1.  Deal'mo.vt,  IV.:  The  Physiology  of  Digestion,  with  Experiments  on 

Ute  Gastric  Juice.  1’IaUsburg,  1833. 

2.  Goodall,  J.  S.:  ‘Appetite:  An  attempted  Analysis  of  the  Psychic 

Factor',  Writ.  Med.  Joum.,  1003,  ii.  5S0. 

3.  Cannon,  W.  I).,  and  Washuurne,  A.  L.;  ‘An  Explanation  of 

Hunger’,  American  Journal  of  Physiot.,  1012,  xxfx,  300. 

1.  Cablso.v,  A.  J. : The  Control  of  Hunger  in  Health  and  Disease.  Uni- 
versity of  Chicago  Press,  1010. 

5.  Rm.vrov,  IV. : Lectures  on  Diseases  of  the  Stomach.  London:  John 
Churchill  & Son,  1801. 

0.  Cull,  11'.:  ‘Anorexia  Nervosa*,  Clinical  Society's  Transactions , 
1871,  \$l.  22. 

7.  Goquuart,  J.:  On  Common  Neuroses,  or  Ute  Neurotic  Element  in 
Disease  and  its  national  Treatment.  Loudon:  II.  K.  Lewi*,  ISO  1. 


IX 

CHRONIC  DIARRHOEA1 

Eon  those  of  us  who  are  chiefly  concerned  with  clinical 
problems  it  is  often  profitable  to  discuss  the  natural  history 
of  a single  symptom;  to  consider  its  several  origins  and 
types ; and  generally  to  pass  in  review  the  diagnostic  diffi- 
culties to  which  it  may  give  rise.  Such  a survey  should 
include  a valuation  of  the  methods  available  for  the  inves- 
tigation of  the  symptom,  and  should  have  as  one  of  its  aims 
the  practical  consideration  of  how  to  rationalize  treatment. 
I have  chosen  as  my  topic  clironic  diarrhoea,  under  which 
heading  may  be  included  recurring  or  intermittent  types 
of  the  complaint.  I shall,  wherever  possible,  base  my  re- 
marks on  personal  clinical  observations,  referring  only  to 
such  special  or  experimental  work  as  seems  to  have  a direct 
and  useful  bearing  on  the  question.  By  diarrhoea  we  should 
imply — to  quote  a formula  of  J.  Cb.  Roux — ‘the  too  rapid 
evacuation  of  too  fluid  stools’,  in  this  way  avoiding  con- 
fusion with  certain  pseudo-diarrhoeas.  So  far  as  its  actual 
incidence  in  practice  is  concerned,  I imagine  chronic  diar- 
rhoea would  not,  in  our  climate  and  at  ordinary  times,  be 
regarded  as  a very  common  symptom.  Nevertheless  it  is  a 
symptom  common  to  a great  variety  of  diseases,  and  it  may 
be  a very  troublesome  one  to  analyse  and  treat.  Further- 
more, by  reason  of  the  wide  extent  of  our  Empire,  increasing 
facilities  for  travel,  and  the  ravages  of  war,  certain  types  of 
infective  diarrhoea  have  undoubtedly  become  more  common 
in  this  country  than  they  were  in  previous  decades. 

For  the  patient  the  symptom  is  mainly  a subjective  one 
— -that  is  to  say,  it  is  the  sensory  discomforts  and  incon- 
veniences which  urge  him  to  seek  advice.  It  has,  however, 
an  advantage  over  more  strictly  subjective  experiences  in 
that  it  is  accompanied  by  the  passage  of  abnormal  stools, 
with  regard  to  the  nature  and  number  of  which  more  or  less 
accurate  observations  are  possible.  In  no  type  of  chronic 

* Lancet,  1624,  ii.  101. 


CHRONIC  DIARRHOEA  131 

diarrhoea  can  we  afford  to  neglect  such  observations.  Some- 
times they  declare  or  suggest  the  diagnosis  at  once.  In  all 
cases  they  give  guidance  as  to  the  necessary  collateral 
inquiries.  There  can  be  no  doubt  that  modern  perfections 
in  domestic  sanitation,  however  great  their  benefits,  have 
served  to  hinder  the  modem  physician,  and  to  render  him 
less  familiar  with  the  appearances  of  normal  and  abnormal 
faecal  discharges  than  were  his  predecessors.  It  will  be 
within  the  experience  of  many  of  us,  too,  that  the  sensi- 
bilities of  the  patient  occasionally  offer  a strong  resistance 
to  our  attempts  to  inspect  a stool.  For  these  and  other 
reasons  the  routine  inspection  and  special  examination  of 
faecal  specimens  have  never  received  the  thorough  attention 
accorded  to  the  urinary  excretions.  I shall  have  occasion 
to  refer  in  more  detail  to  this  matter  as  my  theme  develops. 

Classification 

Before  we  can  discuss  the  several  types  of  diarrhoea 
and  their  differential  features  some  form  of  classification 
is  desirable.  The  best  clinical  classifications  arc  usually 
those  based  on  causal  pathology.  It  so  happens  in  the  ease 
of  chronic  diarrhoea  that  an  anatomical  classification  of  the 
sites  of  origin  of  the  symptom  is  more  convenient,  and  at 
the  same  time  permits  of  a clear  review  of  the  underlying 
morbid  processes.  Thus,  by  considering  in  succession  the 
stomach,  the  small  bowel,  the  large  bowel  and  rectum,  and 
the  accessory  glands  and  structures  communicating  with 
the  digestive  tract  (in  particular  the  pancreas,  the  gall- 
bladder, and  the  absorptive  apparatus  comprising  the 
lactcals  and  mesenteric  glands)  we  cover  the  origins  of 
oil  the  important  varieties  of  chronic  diarrhoea,  with  the 
exception  of  those  depending  on  external  nervous  stimuli 
or  due  to  such  complex  factors  as  obtain  in  the  case  of 
Graves's  disease. 

Those  due  to  nervous  factors  include  a rare  form  of  tabetic 
diarrhoea,  diarrhoea  due  to  reflex  stimulation  from  a neigh- 
bouring visceral  lesion,  and  emotionaJdiarrhoea.  Todiarrhoea 
of  gastric  origin  the  term  gastrogenous  has  l»ecn  applied, 
and  we  might  for  brevity  speak  similarly  of  enterogenous. 


132  CHRONIC  DIARRHOEA 

cologcnous,  pancreatogenous,  psychogcnous  diarrhoea,  and 
so  forth.  Such  adjectives,  however,  are  open  to  criticism 
and  do  not  adequately  indicate  the  cause  of  the  symptom. 
Diarrhoeas  may  also  be  broadly  classified  into  those  depen- 
dent upon  functional  digestive  errors  and  those  dependent 
upon  organic  and  usually  ulcerative  intestinal  disease. 
With  most  of  us  it  will  probably  have  been  a natural  inclina- 
tion to  regard  diarrhoea  as  essentially  a bowel  symptom. 
It  is,  however,  no  more  essentially  a symptom  of  primary 
bowel  disease  than  tachycardia  is  a symptom  of  heart 
disease,  or  dyspepsia  of  stomach  disease.  At  the  outset, 
therefore,  the  classification  which  I have  suggested  reminds 
us  of  the  necessity  in  the  individual  case  of  reviewing 
widely  diverse  possibilities,  and  of  arranging  our  interro- 
gation of  the  patient  in  such  a way  as  to  obtain  information 
relating  to  the  functions  of  many  parts. 

Methods  of  Investigation 

Assuming  a careful  history  to  have  been  taken  and  a 
routine  overhaul  made,  it  becomes  necessary  to  consider 
what  special  examinations  should  be  conducted  in  a given 
case.  These  examinations  may  be  usefully  subdivided  into 
(a)  essential  clinical  examinations;  (6)  valuable  and  often 
essential  accessory  investigations  which  yet  fall  within  the 
scope  and  province  of  the  clinician ; (c)  special  examinations 
for  which  it  is  usually  preferable  to  obtain  the  co-operation 
of  an  expert  in  chemical,  bacteriological,  or  radiographic 
methods. 

The  essential  clinical  examinations  include  inspection 
of  the  stools  and  a rectal  examination,  and  should,  strictly 
speaking,  be  omitted  in  no  case  of  chronic  diarrhoea. 

The  accessory  investigations  falling  within  the  province 
of  the  clinician,  but  in  which  he  may  sometimes  elect  to 
obtain  co-operation,  include  a direct  inspection  of  the 
rectum  or  sigmoid  through  a proctoscope  or  sigmoidoscope; 
a simple  microscopic  examination  of  the  stools  for  blood, 
pus,  meat-fibres,  &c. ; a chemical  examination  of  the  stools 
for  the  presence  of  blood,  or  of  a filtrate  of  the  stools  for 
albumin;  and  occasionally  the  examination  of  a blood  film. 


CHRO.VIC  DIARRHOEA  135 

anaemia,  and  splenic  enlargement  or  a history  of  sore  tongue 
or  of  sensory  manifestations  pointing  to  central  nervous 
disease  should  be  seriously  regarded. 

A fractional  test-meal  in  the  majority  of  cases  shows 
complete  absence  of  free  acid  throughout  the  meal,  and  a 
very  loir  curve  of  total  acidity.  Usually  there  is  rapid 
emptying,  the  stomach  sometimes  being  void  within  a half 
to  three-quarters  of  an  hour  instead  of  In  the  more  usual 
period  of  two  hours.  A rndiographic  examination  with  an 
opaque  meal  shows  a similar  rapid  emptying  and  rapid 
passage  throughout  the  intcstinnl  tract.  This  rapid  evacua- 
tion of  the  stomach,  with  consequent  over-stimulation  of 
activity  in  the  small  intestine  (and  possibly  inadequate 
stimulation  of  the  pancreas)  is  the  likely  cause  of  the 
diarrhoea.  The  therapeutic  test  of  giving  acid  may  be  nn 
important  diagnostic  point  when  other  methods  of  inves- 
tigation arc  not  available. 

The  treatment  includes,  where  possible,  the  removal  of 
any  likely  cause  of  a secondary  achlorhydria,  such  as 
alcoholic  excess  or  dental  sepsis.  An  alcoholic  diarrhoea, 
perhaps  more  commonly  seen  in  beer-drinkers  than  spirit- 
drinkers,  will  improve  or  clear  up  altogether  if  the  patient 
succeeds  in  altering  his  habits,  and  it  can  be  shown  that 
nn  achlorhydria  may  under  these  circumstances  be  replaced 
by  a normal  secretory  curve.  In  gastrogenous  diarrhoea 
doses  as  small  ns  10  or  20  minims  of  the  dilute  preparation 
of  hydrochloric  acid  three  times  a day  may]  be  successful 
in  checking  the  frequent  evacuations,  and  it  is  rarely 
necessary  to  give  more  than  BO  minims.  Taken  with 
lemonade  or  orangeade  with  the  three  main  meals  it  is 
quite  a pleasant  beverage.  I have  also  seen  one  or  two 
cases  of  chronic  diarrhoea,  apparently  of  gastric  origin,  in 
trhieh  complete  relief  Eohatred  the  taking  oE  ttcid,  not  with- 
standing  that  gastric  analysis  gave  normal  figures. 

The  following  case  is  instructive.  In  the  early  stages  the 
patient's  symptoms  were  those  of  a simple  gastric  diarrhoea, 
but  were  not  recognized  ns  such.  Later  he  developed 
Addison’s  anaemia.  The  aceompanjdng  chart  illustrates 
the  test-meal  findings  characteristic  of  both  conditions. 


130  CHRONIC  DIARRHOEA 

A middle-aged  man  came  under  observation  on  account  of  severe 
anaemia,  with  a history  of  breathlessness  and  failing  strength  of 
about  one  year's  duration.  For  nine  years  he  liad  been  troubled  by  a 
chronic  painless  type  of  diarrhoea.  Seven  years  previously  an  X-ray 
examination  had  shown  a rapidly  emptying  stomach  and  exceedingly 
rapid  evneuation  of  the  barium.  The  blood  picture  was  typical  of 
Addison’s  anaemia,  and  the  fractional  test-meal  showed  complete 
achlorhydria.  Within  24  hours  of  starting  to  take  hydrochloric  acid 
the  diarrhoea  was  entirely  controlled. 


II  - )[•— lota!  ad£>r 


Diarrhoea  after  Gastro-cnlerostomy 
One  other  type  of  gastric  diarrhoea  resulting  from  un- 
successful or  too  successful  surgery’  deserves  mention.  From 
time  to  time  one  sees  patients  who  have  had  a gastro- 
enterostomy performed,  and  have  thereafter  developed 
chronic  or  intermittent  diarrhoea.  There  arc  two  types— a 
benign  one  which  is  fortunately  the  more  common,  and  a 
rare  one  associated  with  other  and  graver  symptoms.  The 
benign  type  closely  simulates  the  simple  gastric  diarrhoea 
already  described.  It  is  due  to  a too  patent  stoma  causing 
excessively  rapid  emptying,  with  the  result  that  there  is  no 
time  for  gastric  digestion  to  take  place.  There  is  over- 


CHRONIC  DIARRHOEA  1ST 

neutralization  of  the  gastric  juice,  and  consequently  an 
artificial  achlorhydria;  pancreatic  secretion,  and  certainly 
exposure  to  pancreatic  secretion,  may  also  be  inadequate. 
The  stools  are  light  in  colour,  and  may  show'  fatty  crystals 
and  meat  fibres,  but  no  blood.  There  is  no  pain,  but  there 
is  often  discomfort  referred  to  the  small  bowel  area  sur- 
rounding the  navel  and  occurring  almost  immediately  after 
food.  In  a ease  of  this  kind  recently  under  my  care  the 
patient  had  once  noticed  fragments  of  egg-while  in  the 
stools  within  half  an  hour  of  their  ingestion;  X-rays  showed 
the  stomach  to  be  empty  in  ten  minutes;  test-meal  showed 
achlorhydria,  and  the  stools  contained  soaps,  fatty  acids, 
and  meat  fibres  in  excess  of  normal.  Dry  meals,  lying 
down  after  the  main  meals,  and  the  administration  of  acid 
(provided  there  is  no  persisting  evidence  of  gastric,  duo- 
denal, or  jejunal  ulceration)  often  give  relief. 

The  serious  type  is  due  to  the  development  of  a gnstro- 
jejuno-colic  fistula  ns  the  result  of  secondary  ulceration.  In 
such  eases  pain,  great  emaciation,  foul  eructations,  vomiting 
of  faecal  matter,  and  nnnemia  may  lie  present  in  addition  to 
the  diarrhoea,  and  gastric  acidity  is  likely  to  be  high. 

Diarrhoea  Originating  in  tite  Small  Bowel 

There  is  only  one  important  cause  of  diarrhoea  in  this 
group — namely,  tuberculous  ulceration  of  the  ileum.  For 
this  reason  diagnosis  should  seldom  be  in  doubt  as  (excepting 
in  the  far  Jess  common  variety  of  localized  ileo-caeeal  tuber- 
culosis) there  is  nearly  nlwnys  active  coexisting  lung  disease 
or  generalized  abdominal  tuberculosis.  The  frequency  of  the 
calls  to  stool  is  very  variable,  and  it  should,  of  course,  be 
recognized  that  ulceration  may  be  present  with  constipa- 
tion. Generally  the  frequency  bears  some  kind  of  relation 
to  the  extent  of  the  disease.  A common  story'  is  four  to 
six  actions  daily — a rather  higher  average  figure  than  in 
most  eases  of  gastric  diarrhoea,  but  a lower  one  than  obtains 
in  ulcerative  lesions  of  comparable  severity  in  the  large 
bowel.  In  contradistinction  to  the  gastric  group  pain  is 
a frequent  and  troublesome  association.  It  is  usually 
referred  to  the  peri-umbilical  and  right  iliac  zones,  and 


138  CHRONIC  DIARRHOEA 

tenderness  in  the  right  iliac  fossa  is  commonly  present 
There  is  the  same  post-prandial  tendency  to  looseness  as  in 
the  diarrhoeas  of  gastric  origin,  and  hot  soups  and  fluids 
arc  especially  disturbing.  The  stools  are  soft  or  semi-fluid, 
and  light  in  colour.  It  is  rare  for  macroscopic  blood  or 
mucus  to  be  present,  but  positive  results  with  the  benzi- 
dine, guainc,  and  spectroscopic  tests  arc  obtainable.  If  the 
ulceration  be  very  extensive,  and  particularly  if  there  be 
much  involvement  of  the  mesenteric  glands  causing  obstruc- 
tion to  the  lymphatic  flow,  the  stools  may  be  copious  and 
chalky-looking  and  contain  excess  of  fats  and  soaps,  wliile 
in  virtue  of  the  diarrhoea  undigested  meat  fibres  arc  pre- 
sent. With  appropriate  technique  tubercle  bacilli  can  also 
be  demonstrated. 

Treatment  in  these  cases  can  only  be  palliative,  but  Gull 
[4]  pointed  out  os  long  ago  as  1855  the  importance  of  avoid- 
ing the  then  common  practice  of  giving  cod-liver  oil  or  a 
diet  rich  in  milk  and  cream  in  cases  of  tuberculous  disease 
in  which  fat  absorption  is  at  fault.  Cases  of  diarrhoea  due  to 
a non-specific  enteritis  persisting  long  ofteranattackof  food- 
poisoning arc  occasionally  seen  and  may  be  very  resistant 
to  treatment. 

Diarrhoea  Originating  in  Disease  of  toe  Colon  and 
Rectum 

This  is  a most  important  group,  and  is  more  beset  with 
difficulties  than  either  of  those  to  which  I have  referred. 
It  includes  the  chronic  phases  of  amoebic  and  bacillary 
dysentery,  other  forms  of  infective  ulceration  of  the  colon 
of  unspecified  origin,  non-ulcerative  types  or  stages  of 
colitis,  malignant  ulceration  of  the  colon  and  rectum,  the 
terminal  colitis  of  Bright’s  disease,  certain  spurious  forms 
of  colitis  and  diarrhoea,  such  as  that  which  is  commonly 
classified  as*  nvuco-raembranous’.and  those  due  to  constipa- 
tion, abuse  of  purgatives,  and  excess  of  douching.  In  this 
group  more  than  in  any  other  careful  rectal  examination, 
direct  inspection  of  the  mucosa  through  a sigmoidoscope, 
and  macroscopic  and  microscopic  examinations  of  the 
stools  arc  of  importance.  It  is  in  this  group  that  serious 


CHRONIC  DIARRHOEA.  139 

mistakes  are  made  through  omission  of  simple  examinations. 
It  •will  probably  have  been  within  the  experience  of  many 
of  us  to  discover  a rectal  carcinoma,  primarily  regarded  and 
treated,  sometimes  for  months,  as  a ease  of  ‘diarrhoea** 
‘colitis’,  or  ‘piles’.  I see  two  or  three  such  cases  every  year. 
And  there  are  other  pitfalls;  I have,  for  instance,  in  the  Inst 
two  years  seen  three  patients  who  had  at  some  previous 
date  suffered  from  dysentery  or  ulcerative  colitis,  but  in 
whom  a carcinoma  of  the  colon  had  subsequently  developed 
and  been  missed  in  spite  of  careful  investigations.  The  old 
story  of  colitis  or  dysentery  had  served  to  lull  suspicion 
instead  of  rousing  it,  for  there  is,  I believe,  a definitely 
increased  liability  to  malignancy  in  persons  who  have 
previously  suffered  from  chronic  infective  ulceration  of  the 
large  bowel. 

In  a considerable  proportion  of  all  eases  of  diarrhoea  from 
active  colonic  or  rectal  ulceration,  from  whatever  cause, 
blood,  mucus,  and  sometimes  pus  will  have  been  observed 
by  the  patient  himself  at  some  period  of  his  illness.  So  long 
ns  ulceration  persists  blood  will  be  demonstrable  micro- 
scopically and  chemically,  if  not  mncroscopienlly,  for  the 
cells  liavc  not,  os  in  bleeding  at  a higher  level,  had  time 
to  undergo  disintegration.  Leucocytes  much  more  readily 
undergo  disintegration,  and  for  this  reason  their  presence 
in  large  numbers  points  to  a lesion  low'  down  in  the  large 
bowel  or  to  an  abscess  discharging  thereinto.  Goiffon  (5j 
states  that  albumin  in  the  filtrate  from  a faecal  emulsion  is 
a reliable  index  of  the  presence  of  active  bowel  ulceration, 
but  I have  not  employed  the  test  myself.  I’nin,  both  colicky 
and  (if  there  is  extensive  inflammation  of  the  wall  of  the 
bowel)  more  continuous,  and  accompanied  by  tenderness,  is 
a frequent  but  not  constant  association  of  all  ulcerative 
forms  of  colitis.  It  is  commonly  referred  to  the  lower  ab- 
domen, and  especially  to  the  region  of  the  descending  colon 
and  rectum,  and  is  most  in  evidence  during  or  after  dcfacca- 
tion.  The  diarrhoea  may  be  continuous  or  intermittent 
and,  particularly  in  cases  of  malignant  disease,  may  alter- 
nate with  constipation.  In  an  acute  phase  the  evacuations 
are  frequent  and  small,  and  consist  largely  of  blood. 


HO  CHRONIC  DIARRHOEA 

mucus,  and  sometimes  pus.  In  the  more  chronic  phases 
they  may  be  watery  and  intermixed  with  faecal  material, 
the  blood  and  mucus  being  less  conspicuous.  With  growths 
low  down  in  the  colon  and  in  the  rectum  the  blood  may 
sometimes  be  so  intimately  mixed  with  a watery  brown 
malodorous  evacuation  as  to  escape  the  patient’s  notice. 
When  not  sufficiently  obvious  on  a casual  inspection  blood 
and  mucus  can  often  be  made  apparent  by  gently  tilting 
the  bed-pan — a receptacle  which  should  always  be  em- 
ployed in  preference  to  others  in  suspicious  cases;  the 
viscid  mucous  fragments  are  then  seen  to  slide  more  slowly 
ncross  the  white  field  than  the  fluid  dements  of  the  stool. 
Washing  with  water  mny  also  bring  abnormal  particles  to 
light. 

The  Dysenteries 

In  the  case  of  the  dysenteries  it  is  important  to  recognize 
that  both  varieties  (but  more  rarely  that  due  to  Entamoeba 
histolytica ) may  be  acquired  in  this  country,  and  that  re- 
lapses after  periods  of  good  health  ore  common.  Of  the  two 
the  amoebic  variety  is  the  more  likely  to  give  rise  to  a 
chronic  mild  diarrhoea  with  little  or  no  pain.  The  asylum 
dysenteries  have  been  shown  to  be  generally  due  to  bacillar}’ 
infections,  and  Sir  Arthur  Hurst  [C]  has  suggested  that  a 
considerable  proportion  of  the  sporadic  cases  formerly 
classified  as  ‘ulcerative  colitis*  arc  in  reality  chronic  bacillary 
dysentery.  From  the  point  of  view  of  the  morbid  changes  in 
the  mucosa  no  distinction  can  be  drawn  between  chronic 
bacillary  dysentery  and  chronic  ‘ulcerative  colitis’,  and  a 
certain  proportion  of  cases  of  the  latter  show  a very  remark- 
able response  to  treatment  with  polyvalent  anti-dysentery 
serum.  When  it  is  remembered  that  only  a comparatively 
small  proportion  of  acute  bacillar}’  dysenteries  give  positive 
cultural  results  it  is  no  cause  for  surprise  that  chronic  cases 
are  generally  negative  from  the  bacteriological  standpoint. 
This  uncertainty  in  laboratory  diagnosis  renders  a direct 
visual  examination  of  the  diseased  surface  all  the  more 
important.  So  valuable  diagnostically  is  the  appearance 
of  the  local  lesion  that  a digression  on  the  application  of 


CHRONIC  DIARRHOEA  14! 

sigmoidoscopy  m nil  forms  of  colitis,  whether  suspected  of 
belonging  to  a surgical  or  medical  category’,  may,  perhaps, 
be  pardoned. 

Although,  as  with  other  endoscopic  instruments,  tech- 
nical difficulties  are  encountered  from  time  to  time,  no 
special  manipulative  skill  is  necessary’  for  the  use  of  the 
sigmoidoscope.  It  is  a simple  instrument  and,  with  practice 
and  due  care,  its  employment  entails  little  or  no  risk.  Un- 
less there  is  ulceration  of  the  anal  canal  or  a concomitant 
pelvic  inflammation  its  passage — though  uncomfortable — 
is  practically  pninless  nnd  an  anaesthetic  is  seldom  necessary 
and  should  preferably  not  be  given. 

Unless  general  weakness  or  special  circumstances  forbid, 
the  patient  should  be  examined  in  the  knee-elbow  position. 
There  should  be  as  little  preparation  beforehand  as  possible, 
and  the  clearest  views  arc  often  obtained  in  patients  who 
have  simply  been  instructed  to  get  up  and  empty  the  bowel 
voluntarily  two  or  three  times  in  the  few  hours  before  the 
examination.  Purgatives  arc  best  avoided  altogether,  but 
simple  preliminary  lavage  may  be  necessary'.  A hypodermic 
of  morphine,  20  minutes  before  the  examination,  serves  to 
allay’  anxiety  nnd  to  lesson  peristalsis.  After  the  first  few 
inches  arc  passed  the  instrument  must  be  guided  visually. 

In  ulcerative  colitis  and  chronic  bacillary  dysentery  nil 
phases  between  a granular  mucosa  with  a tendency*  to 
bleed  easily  nnd  extensive,  but  usually  superficial,  ulcera- 
tion may  be  seen.  The  ulcers,  except  in  very  severe  tyqies, 
arc  shallow  nnd  their  margins  arc  not  raised  or  undermined. 
The  intervening  mucosa  is  never  healthy,  appearing  red, 
swollen,  nnd  easily  bleeding.  A film  of  muco-pus  frequently' 
covers  the  ulcerated  areas.  In  eases  of  long  standing  n 
condition  resembling  a generalized  polyposis  may  develop. 

In  the  chronic  forms  of  amoebic  dysentery  seen  in  this 
country*  it  is  rare  to  find  extensive  ulceration;  but  the 
appearances,  though  often  slight  nnd  inconspicuous,  may 
l»e  completely  diagnostic.  The  ulcers  are  usually  quite 
minute  anil  round  nnd  appear  as  tiny  central  craters  in  a 
small  elevation  of  the  mucosa.  The  craters  may  be  empty’ 
or  contain  a yellow  slough,  in  which  ease  they  are  not  unlike 


14.1  CHRONIC  DIARRHOEA 

sometimes  accompany  chronic  constipation  and  the  pro* 

longed  abuse  of  purgatives. 

The  picture  of  muco*mcmbranous  colic  is  a familiar  one. 
It  occurs  in  women  of  a particular  nervous  type  in  whom 
chronic  anxiety  and  depression  have  developed  in  relation 
to  the  state  of  their  excreta  and  many  other  things ; they  are 
generally  of  sallow  habit  and  have  dark  skins;  they  suffer 
much  from  abdominal  pain  referred  especially  to  the  de- 
scending colon,  which  may  be  unduly  palpable  ns  a hard 
cord ; their  evacuations  are  too  frequent  and  they  often  say 
that  they  have  diarrhoea.  Strictly  speaking,  the  stools  are 
too  fluid  only  to  the  extent  that  they  are  passed  in  associa- 
tion with  large  quantities  of  coagulated  mucus  often  in  the 
form  of  long  casts.  If  examined  carefully  and  at  a time  when 
purgatives  arc  not  being  taken,  it  will  generally  be  found 
that  the  faeces  are  fragmentary  and  constipated.  Blood  and 
pus  arc  absent,  and  the  mucous  membrane  appears  normal 
or  only  slightly  red  through  the  sigmoidoscope.  The  con- 
dition is  really  one  of  spasmodic  constipation,  and  the  large 
quantities  of  mucus  are  the  result  of  irritation  and  over- 
secretion rather  than  of  actual  inflammation.  If  treatment 
with  purgatives  or  douches  has  been  carried  out  over  Jong 
periods,  or  there  has  been  much  faecal  retention,  a true 
irritative  colitis  with  diarrhoea  may  be  superadded.  With 
chronic  rectal  constipation  ordyschezia,  erroneously  treated 
with  salts  or  irritating  laxatives,  it  is  not  uncommon  for 
small  ineffectual  fluid  stools  to  be  passed,  but  rectal  and 
abdominal  examination  will  disclose  an  accumulation  of 
scybala  in  the  lower  bowel,  and  discontinuance  of  the 
purgative  medicines  and  the  institution  of  rational  hygienic 
measures  should  relieve  the  condition. 

Diarrhoea  Due  to  Disease  op  the  Pancreas 

Bright  [7]  was  the  first  in  this  country  to  draw  attention 
to  the  occurrence  of  fatty  diarrhoea  in  certain  cases  of 
carcinoma  of  the  pancreas  involving  the  duodenum.  Pan- 
creatic diarrhoea  is  actually  a very  rare  condition,  although, 
mainly  on  the  strength  of  laboratory  reports,  it  has  been  a 
common  diagnosis  in  the  presence  of  steatorrhoea.  The  chief 


CHROMIC  DIARRHOEA  345 

feature  of  the  stools  in  a true  pancreatic  diarrhoea  is  the 
passage  of  fat  in  the  shape  of  oil  or  a fatty  coagulum,  or  of 
oil  which  later  congeals  os  a fatty  layer.  Microscopically 
fat  globules  are  shown  and  undigested  meat  fibres  and  starch 
are  also  present.  The  diastase  test  in  the  urine,  or  glycosuria, 
may  give  further  evidence  of  impaired  pancreatic  function. 
Carcinoma,  calculi,  and  chronic  pancreatitis  ore  among  the 
conditions  in  which  a true  pancreatic  fatty  diarrhoea  h3s 
been  described. 

Fatty  on  Chylous  Diarrhoea  rnosi  Disease  of  the 
Absorptive  System 

There  is,  however,  another  important  cause  of  fatty 
diarrhoea,  as  Gull  [4]  originally  pointed  out,  in  which  the 
fat  is  passed  intimately  mixed  with  the  stools  and  is  largely 
present  as  split  fats,  appearing  under  the  microscope  as 
crystals  and  soaps.  The  stools  under  these  conditions  are 
very  bulky,  in  some  eases  almost  incredibly  so.  They  are 
pultaccous,  pale  or  greyish  in  colour,  greasy  and  rancid, 
and  they  may  froth  like  soap  when  water  is  poured  upon 
them.  The  absorptive  apparatus  includes  the  intestinal 
mucosa  and  the  lacteal  tree.  Gull  recorded  the  occurrence 
of  fatty  stools  of  this  type  in  tuberculous  disease  of  the 
mesenteric  glands,  and  Lecture  X is  concerned  with  similar 
cases  in  which  in  the  course  of  a laparotomy  the  lactcals 
M ere  actually  seen  to  be  enormously  distended  with  chyle, 
owing  to  obstruction  by  caseous  glands  in  the  mesentery. 
Other  conditions  in  which  stools  of  similar  character  may 
be  encountered  include  the  so-called  coeliac  affection  in 
children,  tropical  sprue,  idiopathic  stentorrhoen  (non-tropi- 
cal  sprue),  and  occasional  cases  of  gastro-colic  fistula  nnd 
abdominal  malignant  disease.  In  sprue  nnd  coeliac  disease 
other  symptoms  which  may  accompany  the  fatty  diarrhoea 
of  tabes  mescntcrica  (such  as  tetany  due  to  the  excessive 
excretion  of  calcium)  are  also  recorded,  and  I have,  there- 
fore, put  forward  the  suggestion  that  the  diarrhoea  in  all 
these  conditions  will  probably  be  found  to  lie  due  to  ob- 
struction of  the  lactcals  by  some  other  non- tuberculous 
disease  of  the  mesenteric  glands. 


140  CHRONIC  DIARRHOEA 

The  treatment  of  all  cases  of  fatty  diarrhoea  in  %vhich 
faulty  absorption  is  suspected  should  include  rigid  fat  re- 
striction. It  is  remarkable  what  improvement  in  respect  of 
the  diarrhoea,  weight,  general  nutrition,  and  other  secondary 
symptoms  may  follow  this  simple  procedure. 

Simple  Diarrhoea  accompanying  Mesenteric 
Glandular  Tuberculosis 

In  addition  to  a true  fatty  or  chylous  diarrhoea,  we  should 
also  recognize  a simple  form  of  mild  chronic  diarrhoea  with 
passage  of  light-coloured  stools,  which  is  among  the  earliest 
symptoms  in  tuberculous  disease  of  the  abdominal  lym- 
phatic glands.  The  symptoms  may  be  present  long  before 
the  abdomen  becomes  appreciably  enlarged  or  without  other 
classical  signs  of  tabes  mcsentcrica  ever  appearing.  I have 
seen  several  cases  of  this  type  in  which  further  investiga- 
tions strongly  supported  a diagnosis  largely  prompted  by 
this  symptom.  The  condition  is  practically  confined  to 
children  and  young  adults.  The  following  is  a case  in  point: 

A small  girl,  aged  11,  was  brought  to  see  me  on  account  of  attacks 
of  lower  abdominal  pain.  For  some  time  past  her  mother  had  noticed 
that  she  was  having  her  bowels  moved  too  frequently.  The  stools 
were  reported  os  loose  and  light  in  colour,  and  this  was  confirmed  on 
making  a recta!  examination.  Her  mother  and  teacher  had  both 
observed  that  she  easily  became  tired,  and  she  often  went  to  bed  on 
her  own  initiative  long  before  her  usual  bedtime.  The  pain  in  the 
attacks  was  referred  to  both  iliac  fossae — a common  reference  in  these 
cases.  I suggested  keeping  her  under  observation  at  home,  with 
morning,  afternoon,  and  evening  temperature  records.  The  five 
o’clock  mouth  temperature  (the  hour  at  which  she  often  wanted  to 
go  to  bed)  was  found  to  be  nearly  always  VD  or  above,  and  on  one 
occasion  it  was  100.  X-ray  examination  of  the  thorax  showed 
shadows  of  numerous  small  calcified  glands  at  the  hila,  and  consider- 
able peri-hilar  infiltration.  Rest  in  bed,  with  a diet  In  wliich  fats 
were  kept  low,  resulted  in  a steady  gain  in  weight  and  a cessation  of 
the  diarrhoea.  The  daily  swing  of  temperature  steadily  diminished. 
Tli ere  were  no  further  attacks  of  abdominal  pain.  At  no  period  were 
any  of  the  characteristic  signs  of  tabes  mesenterica  present. 

It  is  improbable  that  the  diarrhoea  in  these  cases  ex- 
presses ileal  ulceration;  I suspect  that  it  signifies  again 
a fault  of  absorption  due  to  glandular  disease,  but  of  a 


CHRONIC  DIARRHOEA  14T 

lesser  degree  than  that  encountered  in  the  occasional  eases 
of  fully  developed  chylous  diarrhoea.  The  diarrhoea  of 
lardnccous  disease — now  so  rarely  seen — probably  depends 
on  faulty  absorption  due  to  amyloid  changes  in  the  intestinal 
mucosa. 

Diarrhoea  in  Chronic  Cholecystitis 
In  chronic  mild  infections  of  the  gall-bladder,  persistent 
or  intermittent  diarrhoea  of  a mild  grade  is  a not  uncommon 
complaint.  The  associated  symptoms  include  epigastric 
or  right  subcostal  pains  and  discomforts;  a dyspepsia  of 
which  nausea  and  right  subscapular  or  intcrscapular  pain 
arc  frequent  features;  vogue  general  ill  health;  n tendency 
to  unexplained  spikes  of  pyrexia  with  other  manifestations 
peculiar  to  chronic  infections  of  the  upper  alimentary  tract. 
There  is  usually  tenderness  at  the  gall-bladder  point.  I ain 
not  sure  whether  the  diarrhoea  in  these  eases  should  be 
regarded  os  a reflex  diarrhoea  akin  to  the  accompanying 
reflex  dyspepsia,  or  os  an  expression  of  the  general  upper- 
tract  infection,  or  possibly  of  the  achlorhydria  which  is 
found  in  a certain  proportion  of  such  cases.  The  treatment 
is  the  treatment  of  cholecystitis.  If  gall-stones  are  not 
suspected  and  there  is  no  sufficient  indication  for  surgery 
it  should  in  the  first  instance  comprise  general  hygienic  and 
dietary  measures,  and  the  administration  of  biliary  anti- 
septics such  ns  urotropinc  nnd  salicylates, 

Diamuioea  Duf.  to  Ojioanic  Nervous  Disease 
I do  not  propose  to  discuss  tabetic  diarrhoea.  French 
authors,  of  whom  Timbal  [0]  mentions  several,  have  de- 
scribed a true  diarrhoea  in  tnl>cs,  hut  I have  not  personally 
seen  a case.  The  only  one  in  my  experience  in  which  the 
diagnosis  might  have  been  entertained  did  not  conform  to 
Roux's  definition;  that  is  to  any,  although  the  patient— an 
undoubted  talietic— complained  of  distressingly  frequent 
and  urgent  calls  to  stool,  she  did  not,  so  far  as  I could  as- 
certain, pass  ‘too  fluid*  stools,  and  more  often  Ilian  not 
she  passed  nothing  at  all.  The  symptom  was,  in  all  prob- 
ability, due  to  true  rectal  or  colonic  crises.  It  had  l»een 


148  CHRONIC  DIARRHOEA 

present  for  many  years,  but  latterly  a change  in  its  character 
had  raised  the  possibility  of  carcinoma  coli.  I did  not  have 
the  opportunity  of  investigating  the  matter  further. 

Reflex  Diarrhoea 

The  following  case  illustrates  a type  of  diarrhoea  which 
may  I think,  legitimately  be  described  under  this  heading. 
Cases  in  which  there  is  an  actual  appendicular  or  pelvic 
abscess  should  not  be  included  in  the  same  category',  for  in 
these  the  sepsis  and  peri-rectal  inflammation  are  the  more 
important  factors. 

A medical  man  who  had  had  bacillary  dysentery  during  the  War 
started  in  1010  to  have  diarrhoea  with  frequently  recurring  exacerba- 
tions, associated  with  much  pain  of  a colicky  character,  but  a com- 
plete absence  of  localizing  signs.  There  was  pyrexia  during  the 
attacks.  Various  Investigations  were  made  with  negative  result.  No 
treatment  had  any  effect.  A very  thorough  investigation  in  a clinic 
between  attacks  was  quite  unproductive,  and  in  1022  it  was  finally 
decided  to  perform  a laparotomy.  A thickened  inflamed  nppendix 
was  removed,  which  contained  about  half  a cubic  centimetre  of  pm. 
There  was  no  subsequent  return  of  the  attacks.  The  appendix  was 
‘silent’  in  so  far  os  the  production  of  symptoms  directing  attention 
to  itself  was  concerned,  but  had  produced  such  definite  bowel  symp- 
toms as  colic  and  diarrhoea. 

Emotional  Diarrhoea 

The  nervous  diarrhoea  which  I wish  more  particularly 
to  stress  expresses  an  anxiety-state,  but  it  is  important  to 
recognize  that  it  may  develop  on  the  basis  of  a true  irritative 
or  infective  diarrhoea.  All  grades  of  it  are  encountered.  One 
individual  may  have  a mere  tendency  to  diarrhoea  at  the 
ordinary  times  of  dcfaecation  or  on  special  stressful  occa- 
sions— as  before  a viva  voce  examination;  another  unfor- 
tunate may  so  far  lose  confidence  in  himself  and  his  power 
to  control  the  activity  of  his  bowel  that  it  becomes  impos- 
sible for  him  to  go  to  any  social  function  or  to  expose 
himself  to  any  conditions  under  which  self-consciousness  is 
likely  to  prevail.  To  have  to  face  the  risk  of  being  out  of 
reach  of  a lavatory  on  these  occasions  becomes  for  him  an 
insufferable  anguish.  The  condition  is  a visceral  neurosis 
closely  akin  to  nervous  bladder  frequency.  Like  stammering 


150  CHRONIC  DIARRHOEA 

The  correctness  of  the  diagnosis  cannot  be  dogmatically 
asserted  in  every  one  of  these  cases,  but  all  were  carefully 
reviewed,  and  most  of  them  were  very  thoroughly  investi- 
gated. Sometimes  more  than  one  factor  may  be  at  work. 
I have,  for  instance,  seen  a case  (not  included  in  this  scries) 
in  which  a relapse  of  ulcerative  colitis  was  associated  with 
gastritis  and  achlorhydria,  attention  being  drawn  to  this 
by  the  presence  of  acne  rosacea. 

I hope  that  I have  said  enough  to  indicate  the  great 
diversity  of  conditions  which  may  give  rise  to  chronic 
diarrhoea,  and  to  suggest  the  methods  most  likely  to  be 
of  sendee  in  their  differentiation.  I have  dealt  with  the 
question  of  treatment  superficially,  but  it  must  be  my 
excuse  that  diagnosis  is  the  beginning  and  the  end  of  medi- 
cine, and  an  essential  preliminary  to  rational  therapeutics. 

REFERENCES 

1.  Bennett,  T.  I.,  and  Ryle,  J.  A.:  Guy' a Hospital  Reports,  1021, 

lxxi.  280. 

2.  Schmidt  v.  Noorden:  Klinik  der  DarmI.rankheiten.  (Verlag  v. 

J.  F.  Bergman.  1021.) 

3.  Ryle,  J.  A.,  and  Baiujer,  H.  W.:  Lancet,  1020,  il.  1105. 

4.  Gull,  IV.:  Guy's  Hospital  Reports,  1855,  i.  SCO. 

5.  Goiffon,  R.:  Manuel  de  Coprologie  Clinique.  (Masson,  Iditeur, 

1921.) 

C.  Hurst,  A.F.:  Guy’s  Hospital  Reports,  1021,  lxxi.  20. 

7.  Bright,  R.;  Medico-Chirurgical  Transactions,  3837,  xviii.  1. 

8.  Ryle,  J.  A.:  Guy's  Hospital  Reports,  1021,  bexiv.  1. 

0.  Timbal,  L.:  Les  Diarrh/es  Chroniques.  (Masson,  £diteur,  1022.) 


152  FATTY  STOOLS  FROM  OBSTRUCTION 

to  be  well  founded,  though  it  ii  probable  they  often  mistook  Inflam- 
matory exudation  for  chyle.  Modem  authors  have  passed  over  the 
subject,  or  have  treated  it  lightly. 

‘The  norma!  absorption  of  fatty  matters  is  prevented  from  two 
causes;  either  from  a defect  in  the  digestive  or  emulsifying  process, 
or  from  disease  of  the  absorbent  system.  The  instances  of  fatty  stools 
from  disease  of  the  pancreas  and  the  duodenum,  as  described  by 
Dr.  Bright  and  others,  belong  to  the  former,  and  arc  characterized 
by  the  fat  passing  from  the  intestines,  more  or  less  separate  from  the 
general  mass  of  the  faeces,  and  concreting  upon  them;  but  in  the 
latter  case,  where  the  disease  is  In  the  absorbent  system,  the  fat, 
being  emulsified,  becomes  incorporated  with  the  evacuation,  and  is  conse- 
quently not  so  easily  recognized.  If,  however,  there  be,  with  defective 
absorption,  an  inflammatory  condition  of  the  mucous  membrane 
and  diarrhoea,  the  oily  matters  rise  to  the  surface  of  the  evacuation 
as  a creamy  film,  and  produce  the  pale,  clialky,  and  soapy  appearance 
so  cliaractcristie  of  chronic  muco -enteritis  and  mesenteric  disease.* 

In  describing  a case  of  fatty  diarrhoea  due  to  tuberculosis 
of  the  mesenteric  glands  he  says: 

‘The  bowels  were  generally  moved  three  times  in  the  twenty-four 
hours.  The  evacuations  were  pultaccous  or  liquid,  of  a dull  chalky 
colour,  frothing  like  soap  when  a stream  of  water  was  poured  on 
them.  Under  the  microscope  they  were  seen  to  contain  muscular 
fibre  in  different  stages  of  disintegration,  starch  cells.  See.,  and  finely 
divided  oily  and  granular  matter  like  chyle,  and  inflammatory  exuda- 
tion.* 

We  can  add  little  if  anything  to  Gull’s  conclusions  as  to 
the  main  causes  preventing  ‘the  normal  absorption  of  fatty 
matters*.  The  interest  which  has  been  stimulated  in  recent 
years  in  the  various  special  tests  for  pancreatic  efficiency 
would  seem,  on  the  experience  of  the  cases  described  here- 
under, to  have  blinded  us  somewhat  to  the  value  of  the 
simpler  methods  of  observation  and  deduction  employed 
by  ‘the  older  physicians’. 

During  the  past  three  years  I have  had  the  opportunity 
of  studying  two  cases  of  fatty  diarrhoea  in  adults,  and  one 
in  a child.  In  both  of  the  adult  cases,  in  spite  of  careful 
clinical  and  laboratory  investigations,  the  true  cause  of  the 
condition  escaped  recognition  prior  to  the  performance  of 
a laparotomy,  and  a diagnosis  of  pancreatic  disease  had 
been  entertained. 

It  should,  I believe,  have  been  possible  in  each  instance 


153 


OF  TIIK  LACTEALS 
to  predict  the  correct  diagnosis  on  clinical  grounds.  I lmve 
therefore  thought  it  worth  while  to  place  on  record  an  ac- 
count of  the  eases  in  question.  In  doing  so  I am  further 
netunted  by  the  fact  that  Case  I showed  features  so  charac- 
teristic of  what  1ms  been  described  as  the  coclinc  disease  in 
children  that  I hoped  tluit  it  might  serve  to  throw  some  light 
upon  the  causal  pathology  of  that  obscure  malady. 

Cash  1.  A young  woman,  need  23.  Admitted  for  chronic  diarrhoea 
and  tetany.  Since  she  was  n baby  ithe  lias  been  subject  to  attacks 
of  diarrhoea.  In  recent  years  these  have  liccome  more  continuous, 
and  latterly  there  has  been  little  or  no  intermission.  Often  she  passes 
six  or  more  fluid  stools  n day.  The  diarrhoea  is  associated  with  pain 
above  the  umbilicus.  In  spite  of  this  prolonged  111  health  she  lias  a 
good  appetite  and  lias  not  lost  weight.  Wien  overtired,  and  in* 
variably  during  the  menstrual  periods,  she  has  attacks  of  true  tetany 
with  earpo-pednl  spasms.  These  liave  been  becoming  worse  and  more 
frequent;  last  from  2 to  0 hours;  and  are  relieved  by  morphine. 
Her  doctor  (Dr.  II.  I».  IJurton)  thinks  they  have  been  fewer  while 
she  has  been  taking  parathyroid  tablet*.  She  looks  younger  than  her 
years;  is  of  small  stature;  and  has  a *plnk  and  white’  complexion, 
with  small  dilated  venules  on  the  cheeks.  The  whole  nlKlomen,  but 
especially  the  lower  part,  is  rather  full  and  tense.  The  abdominal 
reflex  is  brisker  on  the  right.  The  stools  are  enormously  bulky,  fre- 
quently filling  almost  half  an  ordinary  bed-ehamber  as  the  result  of  a 
single  evacuation . They  are  rancid,  greyish  .and  pom’dgy  in  consistency. 
They  thatc  excess  of  fatty  matters  and  m cat  fibres.  Under  the  microscope 
crystals  and  soapy  fragments  xrere  observed.  Quantitative  estimations 
of  the  fat  in  the  stools  were  not  performed. 

Subjective  symptoms  improved  ns  the  result  of  rest.  PancreaUn 
was  given  without  cTTret. 

A few  weeks  after  she  came  under  oWrvntion  tenderness  developed 
In  the  right  iliac  fossa,  and  it  was  decided  to  explore  the  abdomen. 
The  operation  was  performed  by  Mr.  I„  Bromley,  who  reported  ns 
follows;  ‘The  appendix  was  adherent  to  the  lower  end  of  the  mesen- 
tery, It  was  removed  and  found  to  show  n few  scattered  submucous 
haemorrhages,  and  contained  a bend  of  pus  at  its  tip.  The  mesentery 
of  the  smalt  Intestine  contained  innumerable  eases  ting  tolietruloa* 
gland*.  The  lymphatics  rent  looped  and  tortuous,  xrhite  in  colour,  being 
distended  frith  fat  droplets,  the  passage  of  tchieh  era*  obstructed  ly  the 
condition  of  l5e  mesenteric  glands'  Tlte  distended  lacteal*  Indeed 
presented  a remarkable  appearance,  their  calibre  in  places  almost 
equalling  that  of  a tooth-pick.  Their  condition  at  once  explained  the 
nature  of  the  long-standing  fatty  diarrhoea. 

The  patient  was  treated  for  about  a year  with  rest,  open  air,  and  a 
diet  as  nearly  as  possible  f*t-free.  For  a time  there  was  aWetnlnsJ 


154  FATTY  STOOLS  FROM  OBSTRUCTION 

discomfort  find  pain,  and  a small  fluctuating  area  near  the  umbilicus, 
presumed  to  be  due  to  breaking-down  glands,  developed.  Radio- 
graphic evidence  of  peribronchial  glandular  tuberculosis  was  also 
forthcoming,  and  for  n time  some  patches  of  lichen  scrofulosorum 
were  present  on  the  skin.  On  the  fat-free  diet  the  stools  became 
formed  nnd  darker  in  colour,  and  were  reduced  to  one  or  two  per 
diem,  but  they  still  remained  abnormally  bulky. 

Finally  the  patient’s  general  condition  improved  greatly,  and  she 
has  now  been  actively  employed  with  light  duties  for  many  months. 
There  is  no  actual  diarrhoea.  Minor  tetanic  spasms  have  recurred 
from  time  to  time.  Calcium  is  now  being  given  in  an  attempt  to  control 
tliis  symptom.1  Throughout  the  whole  period  of  observation  the 
temperature  only  very  rarely  rose  above  normal.  (Many  years  later, 
after  n life  of  fluctuating  invalidism  always  cheerfully  borne,  this 
patient  died  in  one  of  Sir  Arthur  Hurst’s  beds  at  Guy’s  from  an 
oesophageal  carcinoma.  At  the  necropsy  confirmation  of  the  original 
diagnosis  of  tabes  mesenteries  was  obtained.) 

It  is  difficult  to  avoid  the  conclusion  that  this  patient  had 
a condition  of  tabes  mescnterica  dating  from  early  child- 
hood. For  six  years,  at  any  rate,  she  had  been  subject  to 
tetany,  and  the  diarrhoea  started  many  years  before  tliis. 
Nevertheless,  appetite  and  general  nutrition  had  been  good 
on  the  whole,  and  she  had  been  working  hard  before  coming 
under  observation. 

The  tetany  was  presumed  to  be  associated  with  periods 
of  acute  calcium  deficiency  resulting  from  the  excessive 
excretion  of  calcium  soaps;  it  was  consequently  worse 
when  the  diarrhoea  was  worse,  nnd  disappeared  when  the 
diarrhoea  was  relieved  by  giving  a fat-free  diet. 

The  features  which  might  have  helped  to  establish  the 
diagnosis  were:  (1)  the  naked-eye  appearance  of  the  stools, 
which  were  of  the  bulky,  greasy,  pultaceous  type  described 
by  Gull,  and  contained  no  separate  oil  or  coagulum;  (2) 
the  presence  of  crystals  and  soaps,  suggesting  that  absorp- 
tion rather  than  digestion  was  chiefly  at  fault;  and  (3)  the 
tetany,  which  presumably  should  not  occur  with  the  pas- 
sage of  unsplit  fats  as  in  true  pancreatic  deficiency. 

The  presence  of  meat  fibres  merely  expressed  the  diar- 
rhoeic  state. 

1 5.12.23.  Within  43  hours  of  starting  calcium  lactate,  gr.  x,  three  times 
daily,  minor  facial  and  carpal  spasms,  present  for  some  time,  have  ceased. 
Chvostek’s  sign,  however,  £s  well  marked. 


OP  THE  LACTEALS  155 

Ca.st.2.  A man, aged «lfl.  Admitted  forgrrat  low*  of  weight, hunger, 
thirst,  abdominal  fullness,  nnd  the  passage  of  copious  Ught-colourrd 
stools.  Previous  history:  Preble  nt  birth,  nnd  licfore  the  ngc  of 
17  had  pneumonia,  tuberculous  glands  in  the  neck,  tuberculous 
disease  of  the  left  ankle-joint,  nnd  an  operation  on  the  left  uuvstold 
antrum.  After  the  age  of  18  he  l>cramc  very  fit.  lie  was  always 
a very  large  eater,  hut  his  food  did  not  seem  to  fatten  him.  One  sister 
has  pulmonary  tuberculosis.  He  joined  the  Army  during  the  I914-JS 
War  nnd  served  in  Prance,  Egypt,  and  Salonika.  Append iccctomy 
at  Salonika  in  1015.  In  1020  he  went  to  Canada.  At  this  time  he  was 
feeling  rather  weak  and  had  ‘ocldity'  nnd  lower  otxlominal  discom- 
fort nl>out  1 hour  after  meals.  Next  summer  he  went  away  for  n 
holiday,  and  lived  on  farm  produce,  but  the  aridity  nnd  fullness  in- 
creased rather  thnn  diminished.  In  September  1021  he  had  violent 
diarrhoea  nnd  passed  ten  motions  a day  ‘of  the  colour  of  modellers* 
clay*.  He  was  investigated  in  Toronto,  and  a diagnosis  of  ‘hyper- 
acidity ' was  made.  Another  physician  said  be  had  phthisis,  nnd  a 
third  dysentery.  He  managed  to  remnin  at  work,  but  felt  very  ill 
and  passed  three  stools  a day. 

In  April  1022  he  came  to  England  and  was  re-investigated  in  Lon- 
don. As  the  result  of  various  examinations,  nnd  imrticularly  on  the 
strength  of  the  presence  of  fatty  globules,  fatty  add*,  nnd  meat  fibres 
In  the  stools,  be  was  regarded  as  having  pancreatic  disease.  He  made 
no  Improvement  with  panerrntimt  food  or  pnncrentln.  In  August 
1022,  as  be  was  making  no  headway,  an  exploratory  lajvarotomy  was 
performed  by  Mr.  Cecil  JoM.  A condition  of  tabes  mewmterica  was 
revealed,  nnd,  as  In  the  other  case,  the  lacteal*  were  seen  to  be 
enormously  distended. 

On  admission  in  January  1023  for  further  observation  lie  seas  ter- 
ribly emaciated,  his  weight  having  fallen  from  10  to  7 stone  in  2 
years.  The  abdomen  was  greatly  distended  nnd  tympanitic.  He  was 
suffering  from  an  abnormal  hunger  anil  thirst.  He  expressed  himself 
as  fond  ©r  fats,  cream,  butter,  and  savoury  jellies. 

With  n fat-free  diet,  liberal  fluids,  nnd  pituitary  Injections  to  con- 
trol the  meleorlun,  some  temporary  impros  rnient  was  achieved,  1ml 
It  was  only  too  apparent  tliat  In  addition  to  lacteal  olxlructlon  from 
glandular  disease  the  patient  was  also  suffering  from  tuberculous 
ulceration  of  the  intestine,  and  he  did  not  long  survive. 

In  this  case,  tvs  in  Cnee  No.  1,  the  fallacy  arose  of  suppos- 
ing that  fat  anti  inrnt  fibres  in  the  stools  must  necessarily 
indicate  pancreatic  deficiency.  The  fat  in  each  case  was  due 
to  faulty  absorption  from  obstruction  of  the  Inctealt,  and 
the  meat  fibres  were  merely  nn  expression  of  the  diarrhoea. 

Although  chronic  or  intermittent  diarrhoea  with  light- 
coloured  stools  is  a vreH-rceognlted  symptom  of  tube* 


156  FATTY  STOOLS  FROM  OBSTRUCTION 
mesenterica,  manifestations  of  the  character  and  severity 
seen  in  Cases  1 and  2 must,  I think,  be  rare. 

So  simitar  arc  the  main  symptoms  recorded  in  Case  I to 
those  recorded  in  cases  of  coeliac  disease,  that  I would 
submit  that  the  causal  pathology  of  coeliac  disease  cannot 
be  regarded  as  fully  investigated  until  it  has  been  demon- 
strated at  operation  or  post-mortem  that  there  is,  or  is  not, 
some  obstructive  lesion  in  the  lacteal  system  or  the  thoracic 
duct.  The  lesion  is  most  likely  to  involve  the  mesenteric 
glands.  In  none  of  the  post-mortem  examinations  in  cases 
of  coeliac  disease  referred  to  by  Still  [5]  and  by  Miller  [G] 
is  any  specific  mention  made  of  the  state  of  the  lacteals. 
The  fact  that  the  lacteals  may  be  seen  to  be  distended  at 
operation  on  a patient  taking  a normal  diet  does  not  neces- 
sarily imply  that  they  should  remain  visibly  enlarged  after 
death  in  patients  who  have  been  on  a low  diet  and  have 
died  of  some  terminal  infection.  The  lacteals  were  not 
stated  to  be  so  distended  after  death  in  the  case  reported 
by  Gull,  the  clinical  description  of  which  closely  conforms 
with  the  description  of  Case  2.  Evidence  of  tuberculosis 
has  been  consistently  lacking  in  fatal  cases  of  coeliac 
disease,  but  lymphatic  obstruction  need  not  necessarily  be 
the  result  of  tuberculosis.  In  fatal  cases  of  fatty  diarrhoea 
reported  by  Poynton  and  Paterson  [8]  and  by  Whipple  [9] 
there  was  gross  non-tubcrculous  enlargement  of  the  mesen- 
teric glands,  and  in  Whipple’s  cases  the  glands,  which  were 
fibrotic,  nnd  the  intestinal  villi  were  packed  with  deposits 
of  neutral  fats  and  fatty  acids. 

Miller,  who  is  responsible  for  several  important  contribu- 
tions to  the  study  of  coeliac  disease,  claims  that  there  is  not 
sufficient  evidence  to  indicate  that  the  failure  to  absorb  fats 
is  due  to  any  lesion  of  the  intestinal  mucosa.  He  concludes 
[G]  ‘that  coeliac  disease  is  independent  of  organic  changes 
and  thus  must  he  due  to  a digestive  fault  (probably  a 
defective  action  of  the  bile  on  fat-absorption)  \ That  such 
a gross  derangement  can  depend  upon  ‘a  defective  action 
of  bile  on  fat-absorption  * alone,  when  there  is  no  evidence 
forthcoming  of  hepatic,  biliary,  or  pancreatic  disease,  seems 
to  me  to  be  an  untenable  hypothesis. 


or  THE  LACTEALS  157 

To  replace  it  I would  therefore  put  forward  the  suggestion 
that  the  inability  to  absorb  fats  in  cocliac  disease,  and  the 
attendant  complications,  such  as  infantilism  and  tetany,  can 
best  be  accounted  for  by  an  obstructive  lesion  {probably  infective 
in  origin,  as  the  disease  is  acquired  and  not  congenital)  of 
some  part  or  parts  of  the  lacteal  tree.  The  severity  of  the 
condition  probably  bears  some  relation  to  the  amount  of 
the  obstruction,  and  in  Miller’s  non-diarrhocic  cases  (7j  it 
would  be  reasonable  to  suppose  that  there  is  less  involve- 
ment of  the  mesenteric  glands  than  in  the  fully  developed 
type  of  the  disease.  On  this  hypothesis  also  the  slow  re- 
coveries from  cocliac  disease  might  be  held  to  be  due  in 
part  to  the  establishment  of  a collateral  lymphatic  circula- 
tion, and  the  generally  prompt  improvement  on  a fat-free 
dietary  to  relief  from  overpressure  of  chyle  in  the  already 
choked  lymphatic  tributaries. 

Gee  [10],  in  his  original  account,  apparently  draws  no 
distinction  between  the  cocliac  disease  of  infants  and  those 
tropical  eases  of  fatty  diarrhoea  which  we  now  classify  as 
Sprue.  Manson-Bahr  [11],  in  describing  the  morbid  changes 
found  in  sprue,  says,  ‘The  mesenteric  glands  are  generally 
large  nnd  pigmented,  perhaps  fibrotic.'  He  also  mentions 
the  occurrence  of  tetany  in  chronic  cases,  Decently  attention 
has  been  drawn  by  T.  11.  Jamieson  [12]  to  the  good  results 
obtained  with  a fat-free  dietary  in  sprue,  while  JL  II.  Scott 
[IS]  lias  demonstrated  calcium  deficiency,  and  commends 
the  use  of  calcium  lactate  nnd  parathyroid.  It  seems  highly 
probable  that  the  tetany  nnd  calcium  deficiency  which  occur 
in  .some  eases  both  of  coelinc  disease  nnd  sprue  may  be 
connected  with  the  excessive  excretion  of  calcium  soaps,  ns 
in  Case  1.  Distended  laetcals  have  also  l>een  seen  during 
the  performance  of  laparotomy  in  eases  of  sprue. 

The  following  ease  of  infantilism  nnd  late  rickets  dis- 
played features  strongly  reminiscent  of  cocliac  infantilism. 
The  blood  -calcium  was  deficient,  nnd  although  diarrhoea 
was  only  occasional  there  seat  excess  of  fat  in  the  faeces. 
The  patient  also  show  cd  clinical  ond  radiographic  evidences 
of  tuberculosis,  nnd  1 consequently  suggested  a diagnosis 
of  old  mesenteric  glandular  tuberculosis  causing  faulty  fat- 


158  FATTY  STOOLS  FROM  OBSTRUCTION 

absorption,  and  so  contributing  to  the  retardation  of  growth 
and  the  rickety  bony  changes. 

Casf.  3.  A girl,  aged  1 5,  was  admitted  for* arrest  orgrowtli,  deformi- 
ties, and  intestinal  troubles*. 

At  the  age  of  3}  years  she  Jiad  a febrile  attack  accompanied  by  the 
passage  of  loose  grey  motions.  Attacks  of  this  type  have  recurred 
three  or  four  times  a year  ever  since.  At  10  years  she  only  weighed 
4 st.  5 lb.  Her  appetite  has  always  been  poor,  and  she  will  not  touch 
milk.  The  stools  have  varied  in  character  from  day  to  day,  but  except 
in  the  attacks  there  is  no  diarrhoea.  Patient  is  small,  and  in  hulk  and 
stature  resembles  n child  of  about  8 or  9.  She  is  * old-fashioned*  in 
her  expression  and  behaviour.  There  is  great  enlargement  of  the  ends 
of  the  long  bones,  and  n severe  condition  of  knock-knee.  Weight 
4 st.  1 1 lb.  The  temperature  chart  shows  slight  daily  excursions  above 
the  normal. 

On  a Schmidt's  diet  the  stools  showed  no  excess  of  meat  fibres  and 
no  fat  globules,  hut  60tnc  excess  of  soap  crystals.  On  an  ordinary'  full 
diet  a loose  stool  was  passed  which  showed  a few  fatty  globules,  and 
some  excess  of  soap  crystals. 

Dr.  J.  II.  Ryffcl  reported  quantitatively  on  the  dried  faeces  and 
blood-calcium  as  follows: 

Total  fatty  acid  and  fat  ...  29-54  per  cent. 

Fatty  acid  as  soaps  . . . . . 15  02  „ 

Free  fatty  acid  and  neutral  fat  . . 13-02  „ 

These  figures  arc  distinctly  high  but  bear  normal  relationships. 

‘The  scrum-calcium  was  definitely  though  slightly  low  as  regards 
total  calcium  and  more  so  for  prccipitablc  calcium. 

Calcium  in  ash  of  scrum,  8-9  mg.  per  100  c.c.  {Normal  9-2-10  0). 

Calcium  precipitated  directly  by  oxalate,  7-0  mg.  per  100  c.c. 

(Normal  0 3-0-5  less  than  Ca.  in  ash.)’ 

‘Radiograms  or  the  chest  showed  considerable  enlargement  of  root 
shadows  and  shadows  in  the  right  upper  lobe  suggesth  c of  phthisis.’ 
(Mr.  P.  J.  Briggs.) 

A fat-free  diet  was  prescribed  and,  in  view  of  a low  curve  of  gastric 
acidity,  dilute  hydrochloric  acid  m.  xxx  three  times  a day  with 
meals.  Ten  months  later  the  patient’s  doctor  (Dr.  C.  Ewhank  Lans- 
down)  reported:  ‘Up  to  present  date  she  has  steadily  improved  on 
the  treatment  recommended. . . . There  have  been  only  two  or  three 
slight  set-backs.  There  has  been  no  return  of  the  grey  slaty-coloured 
motions.  She  has  gained  1 st.  8 lb.  in  weight.  The  rickets  has  e to  all 
intents  and  purposes  disappeared.  Muscular  development  has  very- 
much  improved.  She  is  not  like  the  same  child,  being  happy  and 
cheerful  and  developing.’ 

It  is  not  easy  to  collect  information  as  to  the  comparative 
frequency  of  pancreatic  disease  and  disease  of  the  absorbent 


160  FATTY  STOOLS  FROM  OBSTRUCTION  OF  LACTEALS 
an  inflammatory  occlusion  of  some  part  of  the  lacteal  system 
is  responsible  for  the  common  symptoms  in  these  diseases. 

4.  Whether  for  combating  the  main  or  subsidiary  symp- 
toms rigid  fat  restriction  should  play  an  important  part 
in  the  treatment  of  such  conditions  so  long  as  the  stools 
continue  to  give  an  indication  of  mal-absorption  of  fat. 

I am  greatly  indebted  to  Sir  Arthur  Hurst  for  permis- 
sion to  report  upon  the  three  cases  referred  to  above. 

REFERENCES 

1.  The  Extant  Works  of  Aretaeus,  the  Cappadocian,  p.  350.  Edited 

and  translated  by  Francis  Adams:  London.  Printed  for  the 
Sydenliam  Society,  185G. 

2.  O-Si'.n,  L,:  ‘Die  Erkrankungen  des  Ponkreas’,  Nothnagel’s  Spe- 

zielle  Paihologie  und  Therapie , 1808,  xviii.  80. 

3.  Briciit,  R.:  ‘Cases  and  Observations  connected  with  Disease  of 

the  Pancreas  and  Duodenum’,  Medieo-Chinirgical  Transac- 
tions, 1833,  xviii.  1. 

4.  Gull,  IV.:  ‘Fatty  Stools  from  Disease  of  the  Mesenteric  Glands*, 

Guy's  Hospital  Reports,  1855,  i.  800. 

5.  Still,  G.  F.:  ‘On  Cocliac  Disease’  (Lumleian  Lectures),  Lancet, 

1018,  ii.  163, 103,  and  227. 

6.  Mn.i-r.n.  R.:  *A  Fatal  Case  of  Cocliac  Infantilism’,  Lancet,  1921, 

i.  743. 

7.  Milled,  R.,  and  Perkins,  IL:  ‘The  Non-diarrlioeic  Type  of 

Cocliac  Disease’,  Lancet,  1023,  i.  72. 

8.  Poynton,  F.  J.,  and  Paterson,  H.:  ‘The  Occurrence  of  Ascites 

of  a Non-tuber culaus  Origin  in  Chronic  Recurrent  Diarrhoea 
in  Children’,  Lancet,  1014,  i.  1533. 

0 Whittle,  G.  II.:  ‘A  Hitherto  Undescribed  Disease  characterized 
anatomically  by  Deposit  of  Fat  and  Fatty  Acids  in  the  Intes- 
tinal and  Mesenteric  Lymphatic  Tissues’,  Johns  Hopkins 
Bulletin,  1007,  xviii.  382. 

10.  Gee,  D.:  ‘On  the  Coeliae  Affection’,  St.  Bartholomew's  Hospital 

Reports,  1888,  xxiv.  17. 

11.  Manson-Bahr,  P.:  Manson's  Tropical  Disease  (Cassell  & Co.), 

7th  Ed.,  1021,  p.  481. 

12.  Jamieson,  T.  II. : ‘The  Treatment  of  Sprue’,  Lancet,  1023,  ii. 

462. 

13.  Scott,  H.  II.:  ‘The  Treatment  of  Sprue’,  Lancet,  1023,  ii.  870. 

14.  Garbod,  Sir  A.  E.:  ‘The  Diagnosis  of  Disease  of  the  Pancreas’ 

(The  Schorstein  Lecture),  Lancet,  1920, 1.  752. 


XI 

OBSERVATIONS  ON  COLONIC  PAIN1 

Tire  experimental  study  of  pain  in  man,  if  we  except  certain 
superficial  forms  of  pain,  is  clearly  limited  in  its  scope,  and 
it  is  no  matter  for  comment  that  the  subject  of  abdominal 
pain  has  received  a somewhat  scant  attention  in  the  depart* 
meats  of  physiology.  Balloons  and  instruments  may,  it  is 
true,  be  inserted  into  the  stomach,  the  gullet,  and  the 
rectum,  and  the  effects  and  accompaniments  of  certain 
stimuli  have  in  this  way  been  noted  or  graphically  recorded. 
But  there  are  many  organs  and  structures  inaccessible  to 
such  methods  of  inquiry.  Furthermore,  it  hns  not  been 
found  possible  to  reproduce,  even  in  accessible  organs,  the 
many  varieties  and  degrees  of  pain  naturally  peculiar  to 
them,  varieties  and  degrees  which  must  have  a physiologi- 
cal, as  they  undoubtedly  have  their  special  clinical,  signifi- 
cance. The  study  of  visceral  and  corporeal  pains,  ill  suited 
to  the  method  of  experiment,  has  therefore  devolved  largely 
upon  the  physician  and  the  surgeon,  who,  employing  the 
method  of  observation,  must  endeavour  to  gather  and  piece 
together  those  links  in  the  chain  of  evidence  which  the 
physiologist  at  present  seeks  in  vain. 

But  if  the  experimentalist  is  hindered  by  his  lack  of 
opportunity  nnd  material,  the  clinical  observer  is  often 
overwhelmed  by  the  wcnlth  of  his,  nnd  is  further  hampered 
by  the  difficulty  of  imparting  accuracy  to  his  observations. 
Intelligence  and  precision  are  commonly  lacking  in  the 
patients  upon  whom  Nature  performs  before  him  her  experi- 
ments in  pain,  nnd  temperamental  peculiarities  render  the 
assessment  of  pains  most  difficult,  .Morrovrr,  the  problem 
of  accurate  diagnosis  is  ever  present,  and  for  the  study  of 
pain  due  to  a particular  lesion  we  need  not  only  to  know  the 
nature  of  the  lesion  and  iU  situation,  but  also  its  extent,  the 
tissues  invoh'ed,  and  the  character  of  any  associated  de- 
rangements of  function.  It  may  be  said  that  in  the  case  of 

* Gvy'i  //» fj*.  llrpcrti.  1 K»,  Ullt  CVS. 

V 


102  OBSERVATIONS  ON  COLONIC  PAIN 

painful,  malignant,  and  inflammatory  diseases  never,  and  in 
painful  mechanical  disorders  seldom,  does  Nature  provide 
us  Kith  a ‘dean’  experiment.  When  she  produces  visceral 
pain  in  the  absence  of  a lesion  the  scat  of  the  pain  is  com- 
monly invisible  and  impalpable,  and  if  the  organ  is  acces- 
sible to  radiological  or  other  instrumental  survey,  it  may 
happen  that  the  pain  is  in  abeyance  at  the  time  of  the 
investigation. 

It  is  therefore  pertinent  to  ask  whether  there  exists 
any  disorder  commonly  encountered  in  medical  practice  in 
which,  without  demonstrable  organic  disease,  a pain  occurs 
which  is  true  to  type,  and  with  which  there  are  objective 
associations  also  true  to  type  and  of  such  a kind  as  to  suggest 
both  the  seat  of  origin  of  the  pain  and  its  essential  cause. 
A near  approach  to  these  conditions  obtains  in  the  case  of  a 
disorder,  not  extremely  rare,  a cause  of  chronic  or  recurring 
abdominal  pain,  and  one  deserving  of  recognition  if  only 
because  it  leads  too  frequently  to  operations  for  supposed 
organic  disease.  This  disorder  has  been  variously  described 
ns  spastic  constipation,  chronic  colo-spasm,  tonic  harden- 
ing of  the  colon,  and  spastic  colon.  Certain  observations  on 
the  pain  which  is  the  leading  symptom  of  spastic  colon  (I 
use  the  term  for  convenience)  may,  I think,  be  appropri- 
ately reported  here.  Descriptions  of  the  malady  have  been 
furnished  at  various  times  by  Howship  [1],  Cherchewsky  [2], 
Flciner  [3],  Hawkins  [4],  Hurst  [5],  and  Turner  [6].  Stacey 
Wilson  [7]  has  devoted  a book  to  the  subject,  and  I have 
myself  redrawn  the  clinical  picture  in  some  detail.1  I have 
also  described  elsewhere  a simple  system  of  interrogation 
which  has  seemed  to  me  useful  in  the  prosecution  of  any 
clinical  inquiry  into  pain.2  The  ten  questions  included  in 
this  interrogatory  and  the  usual  answers  to  them  given  by 
sufferers  from  spastic  colon  may  be  briefly  recounted. 

The  first  two  questions  are  concerned  with  (1)  the  charac- 
ter and  (2)  the  degree  of  the  pain.  Three  questions  have  a 
bearing  on  spatial  relationships  and  are  answerable  under 
the  headings  of  (3)  situation  (including  depth  from  the  sur- 
face), (4)  localization  (or  extent  of  diffusion),  and  (5) paths  of 
« See  Lecture  NIL  * See  Lecture  III. 


OBSERVATION'S  ON  COLONIC  PAIN  I ta 

reference.  Three  questions  have  a tearing  on  temporal 
relationships  and  arc  answerable  under  the  headings  of 
(G)  duration,  (?)  frequency,  and  (8)  .special  times  of  occur- 
rence or  non-occurrence.  The  two  remaining  questions  arc 
answerable  under  the  headings  of  (9)  aggravating  nnd  (10) 
relieving  factors.  Finally,  it  is  necessary  also  to  review 
associated  symptoms  as  indicating  contemporary  distur- 
bance of  function. 

Tiic  character  of  the  pain  in  spastic  colon  is  usually  a ‘dull, 
steady  ache*,  sometimes  ‘gnawing*,  nnd  never  griping  ns  is 
the  peristaltic  pain  of  purgation  or  obstruction.  It  is  usually 
quite  ‘bearable*,  although  ‘tiring*  nnd  ‘worrying*.  Occa- 
sionally, however,  it  is  of  very  great  severity  and  may  even 
simulate  the  major  ‘colics*  and  require  morphine  for  its 
relief.  Its  situation  is  in  the  course  of  the  ascending,  the 
descending,  or  the  transverse  portions  of  Die  colon,  in  this 
order  of  frequency,  or  in  two  or  all  three  of  these  situations. 
Sometimes  there  is  associated  rectal  pain.  The  localisation 
corresponds  with  the  surface  marking  of  the  colon  nnd  the 
descriptive  gestures  may  be  remarkably  precise.  The  patient 
in  whose  ease  the  appearances  shown  in  Figs.  1 and  2 were 
noted  surprised  her  radiologist  by  accurately  demonstrating 
to  him  the  course  of  her  transverse  colon  on  the  basis  of  her 
sensations.  Sometimes  there  is  a diffuse  lower  abdominal 
reference,  but  more  commonly  the  palm  of  the  right  or  left 
hand  applied  to  the  corresponding  iliac  fossa  or  the  ulnar 
border  of  the  hand  drawn  horizontally  across  the  n)x\omcn 
indicates  the  site  nnd  the  narrow  linear  distribution  of  the 
pain.  I have  not  convinced  myself  of  the  occurrence  of 
referred  somatic  pain  or  tenderness  in  spastic  colon.  The 
pain  is  felt  internally  nnd  has  no  segmental  distribution. 
These  observations  support  the  contention,  based  also  upon 
observations  in  other  abdominal  diseases,  that  referred 
somatic  pain  nnd  tenderness  exprrss  either  a strong  sus- 
tained type  of  stimulus  such  as  inflammation  or  ulceration 
or,  more  rarely,  an  extremely  severe  mechanical  stress  such 
ns  obtains  during  the  passage  of  a calculus,  while  they  are 
usually  absent  or  inconspicuous  in  painful  viverra!  disorders 
of  other  causation.  The  duration  of  the  pirn  is  given  in 


1M  OBSERVATIONS  ON  COLONIC  PAIN 

terms  of  nn  hour  or  hours  or  even  days,  not  in  seconds  or 
minutes  as  in  the  case  of  peristaltic  pain.  Its  frequency  is 
variable,  and  depends  much  upon  the  circumstances  of  the 
patient’s  life  and  general  health.  A special  time  of  occurrence 
is  two  or  three  hours  after  food,  and  of  non-occurrence  during 
the  night,  when,  with  warmth  and  physical  and  mental 
relaxation,  the  pain  departs  and  good  sleep  is  generally  en- 
joyed. Of  aggravating  factors,  cold,  fatigue,  worry,  jolting, 
exercise,  purgation,  and  tobacco  arc  the  most  important. 
Of  relieving  factors,  warmth,  holidays,  belladonna,  and  large 
warm  enemata  arc  noteworthy  examples.  Associated  symp- 
toms include  constipation  frequently,  diarrhoea  less  fre- 
quently, and  intestinal  flatulence.  Gastric  pain,  urinary 
frequency,  dysmenorrhoea,  and  vascular  spasm  as  shown 
by  the  symptom  of  ‘dead  fingers’  arc  also  common  and 
proclaim  the  general  irritability  of  plain  muscle  which 
characterizes  these  cases. 

The  chief  objective  association  is  a palpable  hardening  of 
the  affected  portion  of  the  colon,  which  may  be  felt  through 
the  abdominal  wall  as  a firm  rod  or  sausage-like  tumour. 
This  sign  depends  upon  tonic  rigidity,  shortening  and 
straightening  of  the  affected  loop.  The  same  phenomenon 
may  sometimes  be  witnessed  in  the  course  of  an  abdominal 
operation  when  a loop  becomes  hard  and  pale  and  rigid  in 
the  wound  tlirough  tonic  contraction.  At  the  bedside  the 
degree  of  hardening  may  be  felt  to  vary  under  the  palpating 
hand,  and  I have  known  the  pain  to  become  more  severe 
when  the  hardening  is  extreme  and  to  disappear  with  the 
‘fading’  of  the  ‘lump’.  Often  tender  when  contracted,  the 
bowel  is  less  so,  or  not  at  all,  when  relaxed.  Sometimes  this 
tonic  contraction  extends  to  the  rectum,  and  what  Stacey 
Wilson  [7]  has  aptly  likened  to  a cartilaginous  ring  may  be 
felt  on  digital  examination.  Sustained  ring  contraction  may 
be  observed  during  the  routine  performance  of  sigmoido- 
scopies, but  in  my  experience  it  is  more  pronounced  and 
frequent  in  sufferers  from  spastic  colon.  When  the  lumen 
closes  to  a pin-hole  in  front  of  the  advancing  tube,  the 
patient  may  grunt  and  groan  and  complain  of  lower  ab- 
dominal or  rectal  pain.  The  mucosa  is  normal  in  appear- 


16G  OBSERVATION’S  ON  COLONIC  PAIN 

coat  or  to  the  diminished  vascularity  which  accompanies 
extreme  muscular  contraction  (muscular  ischaemia  from 
arterial  constriction  is  now  held  to  be  the  cause  of  pain  in 
angina  pectoris  and  angina  cruris),  or  to  some  other  cause, 
we  cannot  at  present  say.  Kinsella  [8],  discussing  the  pain 
of  gastric  ulcer,  protests  that  too  much  stress  has  been  laid 
upon  the  muscular  elements  in  the  production  of  gastric 
pain,  and  that  the  local  effects  of  inflammation  have  been 
neglected.  He  appears  to  have  overlooked  the  fact  that 
gastric  pain,  closely  similar  to  and  as  severe  as  the  pain  of 
gastric  and  duodenal  ulcer,  can  occur  in  the  absence  of 
a gastric  or  duodenal  lesion.  I would  submit  that  we  have 
also  in  the  pain  of  spastic  colon  a clear  example  of  a ‘gnaw- 
ing’ or  ‘aching’  viscera!  pain,  sometimes  very  severe,  which 
occurs  in  the  absence  of  any  lesion  of  the  serous,  mucous, 
or  muscular  coats,  but  demonstrably  in  concert  with  sus- 
tained contraction  of  an  abnormal  degree.  Clinical  studies 
indicate  that  this  behaviour  of  the  colon  depends  in  part 
upon  an  inherent  ncuro-muscular  irritability  akin  to  that 
which  is  held  responsible  for  the  bronchial  spasm  of  asthma. 
Like  asthma,  it  is  associated  with  particular  constitutional 
types.  The  two  conditions  may  occur  in  the  same  individual 
or  the  same  family. 

The  pain  of  spastic  colon  is  sufflcientlj'  troublesome  and 
persistent  to  lead  to  diagnoses  of  appendicitis,  gall-stones, 
renal  stone,  ulcer,  and  new  growth.  By  its  character  and 
associations  alone  it  can  frequently  be  distinguished  from 
the  pains  due  to  these  causes.  Its  differentiation  is  practi- 
cally important  both  for  the  avoidance  of  unnecessary 
surgical  procedures  and  as  a basis  for  appropriate  medical 
treatment. 


Summary 

Observations  on  cofonic  pain  have  been  reported  as  con- 
tributory to  the  consideration  of  abdominal  pain  as  a whole, 
and  in  support  of  the  thesis  that  the  pain  of  disease  affecting 
a hollow  viscus  is  experienced  in  the  viscus  and  is  a function 
of  its  musculature;  that  visceral  pain  may  be  localized  with 
considerable  accuracy ; that,  where  inflammation  or  severe 


OBSERVATIONS  ON  COLONIC  TAIN  t«T 

mechanical  stress  is  lacking,  referred  somatic  signs  and 
symptoms  are  generally  absent;  and  that  flic  pain  of 
organic  visceral  disease,  in  itself  evidence  of  a functional 
disturbance,  may  be  closely  simulated  by  the  pain  of  a 
functional  disturbance  without  organic  disease.  It  is  not 
suggested  that  an  abnormal  degree  of  tonic  shortening  or 
hardening  is  the  sole  cause  of  pain  in  the  hollow  organs  of 
the  abdomen,  for  there  nrc  other  stresses,  not  considered 
here,  whereby  tension  in  plain  muscle-fibres  may  be  exag- 
gerated with  resultant  pain. 

m:n:m;.vn^s 

1,  HonMttr,  J.:  Praetiea I llanml.t  on  the  Discrimination  and  Sue- 

restful  Treatment  of  Spasmodic  Stricture  In  the  Colon.  Iy>n«!on, 
1830. 

2.  CiiKRCimwaicr.*  Jin',  tit  .!//</.,  1883,  Hi.  870  nml  1033. 

3,  Ptrrsus,  IV.:  Ilcr tin  Itin.  IVoeh.,  1803,  xxx.  GO  nn«t  0.7. 

4.  IIawxinr,  II.  I*.:  Hrit.  Med,  Joum.,  IOOO,  I.  C5. 

8.  llnnsT,  A.  I*.:  Ccntfip'jit'on  cn/i  Allied  Intestinal  Disorders. 
liOtuion,  1000  nn<l  1010. 

G,  Trnvrn,  P.:  Cw/s  Hasp.  Hep..  1021,  Irxiv.  53, 

7.  Sta(XY  IVmw,  T. : Tonic  Hardening  of  the  Cohn.  Jtandon,  1 027. 

8.  KtVJfELLA,  V.  J.j  lancet,  1020,  il.  1130. 


XII 

CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
AND  THE  DISEASES  WHICH  THEY  SIMULATE1 
Of  the  problems  which  confront  the  physician  and  the 
surgeon  few  are  more  troublesome  than  those  which  require 
the  interpretation  of  chronic  or  recurring  abdominal  pain. 
Frequently  the  diagnosis  must  be  attempted  in  the  absence 
of  any  conspicuous  objective  sign,  and,  with  symptoms 
for  guidance,  a decision  must  be  made  between  ‘organic’ 
and  * functional  or,  what  is  more  serious  for  the  patient  and 
more  exacting  in  clinical  judgement,  between  a surgical  and 
medical  plan  of  relief.  Modem  investigations  do  not  always 
provide  the  clue.  Discussions  which  serve,  in  however  small 
a degree,  to  illuminate  this  dark  field  of  diagnosis  arc  there- 
fore to  be  encouraged,  and  we  should  be  very  ready  to  share 
our  observations  and  our  difficulties. 

However  great  the  triumphs  of  surgery  may  be  in  the 
acute  abdominal  catastrophes  and  in  certain  forms  of 
chronic  abdominal  disease,  none  of  us  can  feel  content  with 
the  present  position  of  abdominal  surgery  as  a whole.  We 
still  see  too  many  scarred  abdomens  with  persistence  of 
symptoms,  too  many  ‘re-operations’  and  operations  under- 
taken for  pain,  and  it  is  disturbing  to  reflect  upon  the  hours 
which  must  be  lost  annually  to  surgeons  and  their  patients 
in  the  conduct  of  unrewarded  appendicectomies,  a con- 
siderable proportion  of  which  have  doubtless  been  advised 
by  physicians.  I would  suggest  that  our  shortcomings  arc 
less  in  respect  of  technique  than  of  diagnosis,  employing  the 
term  in  its  fullest  sense  of  ‘thorough  knowledge’  of  our  cases. 

Such  remarks  as  I shall  have  to  make  are  to  be  regarded 
as  a slender  contribution  to  the  study  of  a not  uncommon 
abdominal  disorder  which  is  characterized  by  frequent  and 
prolonged  discomfort,  or  troublesome  and  even  severe  pain ; 
which  is  unassociated  with  any  demonstrable  organic  change 
in  the  abdominal  viscera ; which  sometimes  simulates  impor- 
1 Lancet,  1928,  iL  1115. 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  169 
tant  organic  disease ; and  for  which  consequently  operations 
and  explorations  are  performed. 

The  condition  is  variously  referred  to  in  the  literature  as 
spastic  constipation,  chronic  colospasm,  spastic  colon,  and 
tonic  hardening  of  the  colon.  For  convenience  I shall  refer  to 
it  as  spastic  colon. 


Historical 

In  Chapter  IV  of  his  Constipation  and  Allied  Intestinal 
Disorders  Hurst  [1]  gives  a useful  bibliography  of  the  sub- 
ject and  a concise  account  of  the  aetiology  and  important 
clinical  features  of  the  malady.  It  was  first  described  by 
John  Howship  [2),  surgeon  to  St.  George’s  Infirmary, 
London,  in  1830,  in  a small  and  very  readable  book  entitled 
Practical  Remarks  on  the  Discrimination  and  Successful 
Treatment  of  Spasmodic  Stricture  in  the  Colon  considered  as 
an  occasional  cause  of  Habitual  Confinement  of  the  Bozcels, 
He  recognized  that  the  complaint  was  due  to  ‘a  deficient 
freedom  of  relaxation  in  some  part  of  the  intestinal  canal 
and  both  as  a diagnostic  test  and  a therapeutic  measure 
advocated  gradual  distension  of  the  bowel  with  a large 
warm  gruel  enema.  Cherchewsky  [8],  who  was  unfamiliar 
with  this  account,  redescribed  the  condition  in  1833.  Fleiner 
(4]  wrote  his  first  article  on  spastic  constipation  in  1898. 
In  this  country  Hawkins  [5]  wrote  an  admirably  descriptive 
paper  based  on  the  study  of  35  cases  of  enterospasm  in  1906, 
drawing  particular  attention  to  the  frequent  confusion  of 
the  disease  with  appendicitis.  The  subject  has  hitherto 
attracted  more  attention  on  the  Continent,  but  latterly  there 
has  been  a revival  of  interest  in  England.  Turner  [6],  from 
the  surgeon’s  point  of  view,  furnished  an  article  to  the 
Guy's  Hospital  Reports  in  1924.  Dr.  G.  Evans  made  it  the 
subject  of  a communication  to  the  Association  of  Physicians 
of  Great  Britain  and  Ireland  In  1928.  Stacey  Wilson  [7,  8J, 
who  had  previously  discussed  the  physiology  of  the  pain  in 
this  disorder,  has  summarized  his  own  views  and  wide  ex- 
perience in  a book  entitled  Tonic  Hardening  of  the  Colon. 
In  this  he  discusses  clinical  features  and  advances  his  own 
therapeutic  beliefs,  but  attributes,  in  my  opinion,  too  long 


170  CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
a list  of  physical  and  mental  disturbances  to  the  direct 
agency  of  tonic  hardening. 

The  Clinical  Pictube  of  Spastic  Colon 
The  descriptions  which  follow  arc  based  on  an  analysis  of 
SO  cases  interrogated  and  examined  by  myself.  The  series 
includes  09  cases  of  spastic  colon  unaccompanied  by  an 
excess  of  mucus  in  the  stools  and  11  cases  of  the  condition 
usually  called  muco-mcmbranous  colitis,  or,  better,  mucous 
colic  or  muco-mcmbranous  colic,  for  cytological  examina- 
tion of  the  stools  and  the  sigmoidoscope  reveal  no  signs  of 
ulceration  and  little  or  no  evidence  of  active  inflammation 
of  the  mucosa.  The  cases  were  taken  from  my  files  consecu- 
tively and  with  no  special  selection,  excepting  that  those  in 
which  there  was  an  element  of  doubt  or  obvious  coinci- 
dental disease  were  excluded.  The  proportion  of  ‘spastic 
colon*  cases  to  cases  of  ‘mucous  colic*  is,  I believe,  repre- 
sentative. The  more  detailed  consideration  of  aetiology, 
symptoms,  and  physical  signs  is  preceded  by  an  account  of 
an  individual  case  portraying  the  more  important  features. 

Case  1 . A middle-aged  professional  man,  of  Jean  type  and  nervous 
constitution  and  liable  to  migraine,  first  started  to  have  right -sided 
abdominal  pain  some  10  years  ago.  At  one  time  and  another,  chole- 
cystitis and  appendicitis  were  diagnosed,  and  finally,  artcr  careful 
investigation,  the  appendix  was  removed.  He  still,  however,  has  the 
right-sided  pain,  and  at  times  can  feel  for  himself  a sausage-like  Jump 
in  tlie  right  flank.  The  attacks  arrive  especially  in  spring  and  autumn, 
and  are  precipitated  by  cold,  fatigue,  and  mental  worry.  In  a hot 
bath  the  pain  is  eased  and  the  tumour  fades  away.  The  patient  and 
his  brother  arc  both  unable  to  face  a cold  east  wind  without  develop- 
ing abdominal  pain.  The  pain  shows  a tendency  to  appear  2J  hours 
after  a meal.  Examination  revealed  general  right-sided  tenderness, 
and  on  one  occasion  the  caecum  or  ascending  colon  became  vaguely 
palpable.  The  descending  colon  was  felt  like  a firm  cord,  and  occa- 
sionally the  transverse  colon  was  also  felt.  There  were  no  other  signs 
of  disease.  The  patient  found  that  a good  open-air  holiday  with 
exercise  and  mental  rest  was  best  calculated  to  bring  relief.  At  a later 
date  he  developed  a duodenal  ulcer. 

Aetiology  of  Spastic  Colon 
Sex  Incidence. — In  the  present  series  of  50  cases  there 
were  17  males  and  33  females.  Excluding  the  cases  with 


CHRONIC  SPASMODIC  AFFECTIONS  OF  TIIE  COLON  171 
mucous  colic  which,  with  rare  exceptions,  are  confined  to 
the  female  sex,  there  were  1C  males  and  23  females. 

Age  Incidence. — The  youngest  patient  was  aged  19,  the 
oldest  78.  The  average  age  was  39. 

Physical  and  Psychological  Types. — Nineteen  cases  were 
specifically  described  in  my  notes  as  ‘lean’,  ‘thin’,  or 
‘spare’.  ‘Wiry’,  ‘dark’,  ‘tali’,  and  ‘pale’  were  other 
adjectives  which  occurred  with  conspicuous  frequency. 
Twenty-seven  cases  were  recorded  as  nervous,  neurotic, 
worrying,  or  anxious.  Migraine  and  asthma  were  entered 
against  the  patient  or  an  immediate  relative  with  sufficient 
frequency  to  suggest  a more  than  coincidental  association. 
The  association  with  asthma  is  commented  upon  by 
Hawkins  [5], 

Family  History. — In  addition  to  these  associations  and 
general  references  to  *ncnous  stock’  there  were  tiro  ex- 
amples in  my  series  of  two  brothers  both  suffering  from 
spastic  colon. 

The  evidence  for  a constitutional  or  diathetic  factor  is 
thus  fairly  strong,  and  has,  I think,  usually  been  remarked 
by  those  interested  in  the  condition.  Conversely  I would 
suggest  that  it  is  extremely  rare  to  meet  with  spastic  colon 
in  fair-haired,  blue-eyed,  healthy-complcxioned  types  with 
placid  dispositions  or  in  robust  individuals.  In  my  own 
experience  spastic  colon  is  more  common  in  private  than  in 
hospital  practice.  As  Hawkins  remarks,  ‘Intestinal  neuroses 
diminish  in  frequency  as  we  descend  the  social  scale.’ 

Predisposing  Illnesses  and  Intoxications. — Dysentery , as 
might  be  expected  from  the  habit  of  irritability  which  it 
engenders  in  the  bowel,  may  be  followed  by  spastic  colon, 
and  tins  even  for  years  after  the  active  infection  lias  sub- 
sided. Three  cases  occurred  in  my  series.  Hurst  also  refers 
to  the  influence  of  lead  and  tobacco,  and  to  colonic  spasm 
reflexly  induced  by  gall-stones,  ureteric  calculus,  or  other 
irritative  visceral  lesions,  or  due  to  tabes  dorsalis.  It  is 
very  difficult  to  assess  the  part  played  by  tobacco.  I would 
suggest  that  it  is  rarely  the  sole  or  main  factor.  Most  of  my 
male  patients  were  smokers,  and  four  of  them  really  exces- 
sive smokers.  On  the  other  hand,  the  majority  of  the  women 


172  CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
were  non-smokers.  Occasionally  I have  seen  patients  with 
spastic  colon  in  association  with  other  manifestations  of 
tobacco  excess,  such  as  sweating,  dizziness,  and  palpitation. 
Plumbism  and  such  coincidental  diseases  as  appendicitis, 
diverticulitis,  gall-stones,  and  tabes  were,  so  far  as  possible, 
excluded.  The  causal  or  contributory  effect  of  purgatives 
must  be  given  due  prominence.  Thirty  of  the  cases  were 
recorded  ns  constipated,  and  of  these  the  majority  were 
taking  laxatives  or  purgatives  occasionally  or  habitually. 
It  cannot  be  doubted  that  undue  irritability  of  the  neuro- 
muscular mechanism  of  the  bowel  is  present  in  these  cases, 
and  that  the  majority  of  the  popular  purgatives,  however 
mildly  so,  are  irritants.  Furthermore,  not  a few  of  the 
patients  are  well  aware  that  their  pain  may  be  aggravated 
by  purgation. 

Constipation. — How  far  constipation  is  to  be  regarded  as 
a cause  or  a consequence  of  the  spasm  it  is  difficult  to  say, 
but,  as  already  mentioned,  it  was  present  in  30  (CO  per  cent.) 
of  the  cases.  Nevertheless  it  is  important  to  recognize  that 
pain  and  tonic  hardening  of  the  colon  are  consistent  with 
regular  and  apparently  normal  bowel  {unction.  Attacks  of 
‘diarrhoea’  are  a constant  feature  in  mucous  colic.  Diar- 
rhoea, occasional  or  constant,  was  also  recorded  in  7 cases 
of  simple  spastic  colon.  In  some  cases,  both  costive  and 
otherwise,  it  is  tempting  to  believe  that  a low-grade  colonic 
infection  is  at  work,  but  we  have  no  certain  information  on 
this  point.  The  cases  are  not  pyrcxial. 

Frequency  of  Previous  Afpendicectojiy 

In  18  (30  per  cent.)  of  my  cases  the  appendix  had  been 
removed.  In  one  of  these  it  was  removed  during  a laparo- 
tomy which  I myself  advised  (vide  Case  S).  In  only  three 
instances  was  it  specifically  noted  that  the  appendicec- 
tomy  was  undertaken  for  acute  appendicitis.  In  several 
instances  the  operation  was  undertaken  for  relief  of  pain 
not  dissimilar  from  that  for  which  relief  was  again  sought. 
In  one  case  there  had  been  two  further  explorations.  In 
other  cases  a diagnosis  of  ‘chronic  appendicitis*  had  been 
suggested. 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  178 


The  Patient’s  Symptoms 

The  leading  complaint  is  usually  of  discomfort  or  pain  in 
the  lower  abdomen.  The  discomforts  are  variously  described 
as  a feeling  of  stagnation  or  ‘stoppage’,  as  ‘a  ball’  or  ‘a 
lump’,  or  as  a sensation  * like  a bar  of  lead’ ; the  direction  of 
this  bar  may  actually  correspond  with  some  part  of  the  large 
bowel,  and  the  description  is  remarkable  for  the  nicety  with 
which  it  interprets  the  tonic  rigidity  present  in  the  affected 
segment.  The  pain  is  usually  a dull  continuous  ache,  some- 
times ‘gnawing’  or  ‘like  a toothache*,  never  rhythmical  or 
griping  as  in  the  colic  of  purgation,  acute  enteritis,  or  in- 
testinal obstruction,  and  even  in  the  severe  cases  unlike 
the  shnrper,  immobilizing  pain  of  an  acute  inflammatory 
lesion.  It  varies  in  severity  from  something  quite  trivial  to 
an  intensity — as  will  be  described  later — so  severe  as  to 
simulate  the  major  colic  of  a ureteric  calculus,  and  to  call  for 
the  administration  of  morphine.  These  severe  cases  arefortu- 
nately  rare.  Diagnosis  even  in  the  attack  may  be  extremely 
difficult.  In  a case  of  average  severity  the  pain  is  at  times 
troublesome  enough  to  interfere  seriously  with  work  or 
pleasure,  although  it  is  noteworthy  that  sleep  is  seldom  lost 
on  account  of  it.  It  is  usually  referred  with  accuracy  to  the 
part  of  the  colon  involved,  and  I must  differ  from  Stacey 
Wilson  [7,  8]  when  he  states  that  the  distribution  is  seg- 
mental. A common  gesture  is  the  application  of  the  palm  of 
the  right  or  left  hand  to  the  corresponding  iliac  fossa,  when 
the  proximal  or  distal  portions  are  affected.  In  the  case 
of  the  transverse  colon  the  course  of  the  pain  is  traced  ■with  a 
finger  or  shown  with  the  ulnar  border  of  the  hand.  For  pur- 
poses of  brevity  I tabulated  the  caecum  and  ascending  colon 
as  'first  part';  the  transverse  colon  as  'second  part’;  and 
the  colon  from  the  splenic  flexure  to  the  commencement  of 
the  rectum  as  ‘third  part’.  Of  the  cases  in  which  observa- 
tions of  the  part  affected  were  noted  the  first  part  was  indi- 
cated in  26,  the  second  in  14,  and  the  third  in  21.  Bectal 
pain  was  also  recorded  in  a few  cases.  Some  patients  could 
only  describe  a vague  lower  abdominal  ‘stomach-ache*. 
Variations  in  the  situation  of  the  pain  are  spontaneously 


174  CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
described.  Associated  pyloric  spasm  and,  in  women,  bladder 
discomfort  and  frequency  are  not  rare.  ‘Dead  fingers’  are 
a common  complaint.  With  the  pain  there  is  often  mental 
depression  or  irritability  and  physical  inertia.  Both  onset 
and  relief  may  be  abrupt  and  occur  for  no  apparent  reason. 
The  duration  of  the  pain  varies  from  an  hour  or  less  to  many 
hours  or  even  days. 

Of  aggravating  or  precipitating  factors  I would  particu- 
larly mention  cold  and  fatigue,  each  of  which  was  speci- 
fically recorded  in  14  instances ; jolting,  such  ns  results  from 
games  or  digging,  horse-riding  or  motoring  over  rough  roads, 
and  even  walking;  mental  stress  or  worry;  purgatives; 
tobacco;  and,  in  women,  the  menstrual  cycle.  The  more 
irritable  cases  of  mucous  colic  arc  very  susceptible  to  fruit. 
Patients  are  sometimes  more,  sometimes  less,  comfortable 
when  their  bowels  arc  confined,  but  aggravation  of  pain 
immediately  after  the  act  of  dcfaecation  is  common.  Warmth, 
rest,  hot  baths,  and  open-air  holidays  with  freedom  from 
cares  are  among  the  relieving  factors.  Food  sometimes  gives 
temporary  relief. 

Piiysical  Findings 

To  these  disturbed  sensations  certain  objective  informa- 
tion can  be  added  in  a high  proportion  of  cases,  more 
especially  if  the  opportunities  for  examination  are  frequent. 
The  physical  sign  of  the  disease  is  an  unusual  palpability  of 
some  part  or  parts  of  the  colon;  this  depends  upon  tonic 
rigidity,  shortening  and  straightening  of  the  affected  loop. 
The  colon  can  often  be  felt  in  the  left  iliac  fossa  in  healthy 
persons  or  in  patients  without  colonic  disease,  and  simple 
palpability  in  this  region  cannot  be  regarded  os  pathological. 
In  spastic  colon  it  is  felt  as  an  unduly  hard  cord  of  small 
calibre.  It  is  doubtful  if  the  colon  is  ever  palpable  in  its 
proximal  or  transverse  portions  in  perfect  health.  In  the 
condition  of  spastic  colon,  however,  either  of  these  portions 
may  be  felt  as  a firm  rod  or  sausage-like  tumour.  This  is 
sometimes,  but  by  no  means  always,  tender.  The  degree  of 
palpability  varies  from  time  to  time,  and  even  in  the  course 
of  a single  examination,  and  is  more  likely  to  be  remarked 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  175 
when  symptoms  are  present.  In  those  cases  in  which  undue 
palpability  was  noted  in  my  series  the  first  part  was  affected 
in  18  instances,  the  second  part  in  8,  the  third  part  in  9. 
The  first  and  third  parts  were  simultaneously  felt  in  8,  and 
all  three  parts  in  4 cases.  What  Stacey  Wilson  aptly  likens 
to  a ‘cartilaginous  ring*  may  sometimes  be  felt  on  inserting 
the  finger  into  the  rectum.  Occasionally  attacks  of  balloon' 
ing  of  the  caecum  are  observed  behind  a spastic  ascending 
colon. 

The  stools  os  a rule  show  nothing  very  characteristic 
excepting  in  the  group  to  be  separately  considered  under 
the  heading  of  mucous  colic.  In  the  larger  group  there  is  no 
mucous  excess  or  occasional  very  slight  excess ; no  blood ; and 
the  colour  \’aries  within  normal  limits.  There  may,  however, 
be  fragmentation,  and,  in  the  presence  of  anal  spasm,  nar- 
rowing of  the  faecal  mass.  If  purgatives  are  being  used  the 
motions  may,  of  course,  be  ‘loose’,  ‘messy’,  and  unsatis- 
factory. 

Sigmoidoscopy  is  often  both  difficult  and  painful  on 
account  of  spastic  narrowing  of  the  rectal  and  sigmoid 
lumen  which  is  further  stimulated  by  passage  of  the 
instrument.  Fluctuations  in  the  degree  of  spasm  can  be 
witnessed  simultaneously  with  variations  in  the  pain  com- 
plained of  by  the  patient.  The  mucosa  looks  perfectly 
healthy. 

Less  is  to  be  gleaned  from  X-ray  examination  than  might 
be  supposed.  In  the  first  place,  the  spastic  state  is  intermit- 
tent and  may  not  coincide  with  the  examination.  In  the 
second  place,  a barium  enema,  which  is  commonly  used  in 
preference  to  the  barium  meal  in  colonic  cases,  may,  by  its 
gradual  introduction  and  gentle  distension,  overcome  exist- 
ing spasm,  just  as  Howship  was  able  to  overcome  painful 
spasm  with  a large  gruel  enema;  in  the  third  place,  when 
views  are  taken  after  evacuation  of  the  bulk  of  the  meal  or 
enema,  it  is  necessary  to  distinguish  the  appearances  of  a 
normal  but  partly  emptied  segment  from  a segment  with 
spastic  narrowing  of  its  lumen.  Examination  after  a barium 
meal  is  more  likely  to  give  positive  evidence.  In  extreme 
cases  the  affected  length  of  bowel  nppears  as  a thin  thread 


176  CIIRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
or  streak  of  barium,  sometimes  with  a sharp  line  of  demarca- 
tion from  the  better  filled  portions.  Normal  haustrations, 
deepened  with  lesser  degrees  of  spasm,  become  obliterated 
when  the  spasm  is  very  pronounced.  In  some  cases  the 
whole  transverse  or  descending  colon  or  a longer  portion  is 
involved ; in  others,  but  less  frequently,  the  spasm  is  loca- 
lized to  an  inch  or  two.  The  localized  spasms  cause  a more 
intense  pain.  Two  other  departures  from  the  normal  ore 
important  and  will  be  discussed  later.  These  are  shortening 
and  straightening  of  the  affected  loop. 

Mucous  on  Muco-jiembranous  Colic 

{Muco-mcmbranous  Colitis) 

I sec  no  valid  reason  for  placing  these  cases  in  a separate 
category.  The  abdominal  pains  described,  the  aggravating 
and  relieving  factors  and  the  radiographic  appearances  are 
identical.  The  chief  differences  are  as  follows:  (1)  the  sex 
incidence,  the  cases  being  almost  all  in  women;  (2)  the 
passage  in  attacks  (usually  after  a period  of  constipation, 
chilling,  anxiety,  or  fatigue)  of  large  quantities  of  coagulated 
mucus,  sometimes  in  costs  or  shreds  or  enveloping  small 
scybalous  fragments ; (3)  the  more  evident  neurotic  associa- 
tions; (4)  an  exaggerated  colonic  tenderness  with  flinching 
and  hyperalgesia,  but  less  definite  palpability  of  the  bowel. 
The  sigmoidoscopic  findings  are  as  described  in  simple 
spastic  colon.  The  mucosa  is  smooth,  and,  at  the  most, 
slightly  redder  than  normal. 

Dittebential  Diagnosis 

Judging  by  my  own  difficulties  and  those  experienced  by 
colleagues  who  have  referred  cases  to  me,  the  following 
conditions  are  among  those  which  are  simulated  or  sug- 
gested by  the  ‘spastic  colon’ : (1)  appendicitis,  acute  and 
chronic,  (2)  duodenal  ulcer,  (3)  diverticulitis,  (4)  colonic 
carcinoma,  (5)  renal  colic,  (C)  intestinal  obstruction,  (7) 
ovarian  or  tubal  disease,  (8)  neurasthenia  and  hypochon- 
driasis, (0)  faecal  tumours.  Finally  (10)  the  cases  with 
mucous  excess  seem  not  infrequently  to  conjure  doubts 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  177 
about  the  possibility  of  ulcerative  colitis,  or  have  been 
vaguely  classified  as  ‘colitis’. 

(1)  Appendicitis.  In  one  of  my  cases  the  hard  lump  in 
the  right  iliac  fossa  formed  by  the  contracted  colon  during 
an  attack  of  pain  had  led  a surgeon  to  a provisional  dia- 
gnosis of  appendicular  abscess.  More  usually  the  persistence 
of  symptoms  leads  to  appendicectomy  for  a so-called  ‘ grum- 
bling appendix*.  In  simple  spastic  colon  there  is,  as  a rule, 
no  pyrexia,  guarding,  vomiting,  or  cutaneous  hyperalgesia. 
In  acute  exacerbations  of  mucous  colic  there  may,  however, 
be  slight  pyrexia,  flinching  (rather  than  guarding),  super- 
ficial soreness,  deep  tenderness,  and  even  sickness;  but  the 
previous  history,  the  patient’s  psychology,  and  inspection 
of  the  stools  generally  establish  the  diagnosis.  In  simple 
spastic  colon  the  interrogation,  particularly  in  regard  to  the 
nature,  duration,  and  localization  of  the  pain,  and  careful 
palpation  along  the  course  of  the  colon  are  usually  adequate. 
(2)  Duodenal  ulcer  may  be  simulated,  firstly,  because  of 
associated  pyloric  or  gastric  spasm  with  food  relief;  and, 
secondly,  because  the  colonic  pain  itself,  although  differently 
situated,  may  develop  late  after  meals  and  be  relieved  by 
food.  The  two  conditions  may  also  occur  together.  If 
there  is  any  suspicion  of  duodenal  ulcer  as  an  alterna- 
tive or  additional  diagnosis  a full  investigation  should  be 
advised.  (3)  Diverticulitis.  In  the  left-sided  cases  particu- 
larly this  possibility  must  be  borne  in  mind,  but  the  type  of 
individual  affected  is  usually  different,  the  victim  of  diver- 
ticulitis being  commonly  well  nourished  and  Jess  commonly 
neuropathic.  The  inflammatory  tenderness  and  thickening 
of  pericolitis  and  pyrexia  during  exacerbations  are  distinc- 
tive. X-ray  examination  after  a barium  enema  should  be 
made  in  case  of  doubt.  (4)  Colonic  carcinoma  has  frequently 
been  feared  in  cases  of  spastic  colon  because  the  patient 
himself  or  his  physician  has  discovered  a hard  lump  in  the 
course  of  the  colon.  The  smoothness  of  the  tumour,  its 
sausage-  or  rod -like  formation,  its  mobility  in  the  case  of 
the  ascending  or  transverse  colon,  its  variations  in  size  and 
hardness,  or  complete  disappearance  under  observation  or 
in  a hot  bath  are  helpful  points  in  differentiation.  The 


178  CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
absence  of  obstructive  symptoms  on  the  one  hand,  and  of 
diarrhoea  or  passage  of  blood  on  the  other,  and  generally  a 
very  long  history  of  abdominal  discomforts  are  reassuring 
features.  If  doubts  persist  the  aid  of  the  radiologist,  sig- 
moidoscopy, and  chemical  and  cytological  examination  of 
the  stools  should  be  invoked.  (5)  Renal  colic  is  only  likely 
to  be  simulated  in  the  occasional  cases  with  very  severe 
pain  ( vide  Case  3,  in  which  the  hardened  colon  was  mistaken 
by  myself  and  others  for  the  left  kidney).  (0)  Intestinal  ob- 
slruction  was  feared  in  Case  4,  in  which  the  complication  of 
caecal  distension  was  present.  (7)  Ovarian  or  tubal  disease. 
At  one  time  it  was  not  uncommon  for  operations  on  one  or 
both  ovaries,  but  especially  the  left,  to  be  performed  for 
spastic  colon.  The  fallacy  probably  arose  from  the  aggrava- 
tion of  colonic  pain  which  sometimes  accompanies  the  period 
and  from  the  association  with  dysmenorrlioca.  (8)  Neuras- 
thenia and  hypochondriasis  may  nppear  appropriate  labels 
in  some  cases  of  spastic  colon,  but  they  do  not  embody  an 
adequate  explanation  of  the  pain  and  physical  findings. 

(9)  Faecal  accumulations  can  be  disposed  of  with  enemata. 

(10)  ‘ Colitis ’ is  an  inaccurate  pathology.  I have  had  several 
cases  of  mucous  colic  referred  to  me  with  a diagnosis  of 
ulcerative  colitis,  but  the  two  conditions  bear  little  resem- 
blance to  one  another.  In  the  more  serious  disease  an  ill 
and  frequently  anaemic  and  wasted  patient  gives  a history 
of  watery  diarrhoea  and  passing  blood  and  mucus,  com- 
monly with  a febrile,  dysenteric  onset.  The  diagnosis  is 
completed  with  the  sigmoidoscope. 

Frequency  of  Spastic  Colon 
Taking  all  grades  of  the  condition,  allowing  for  its  varied 
appellations  and  deceptions,  and  judging  by  information 
received  from  colleagues  in  general  practice,  I can  only 
conclude  that  spastic  colon  is  a common  disorder.  On  the 
basis  of  consulting  and  hospital  experience  I should  say  that 
it  ranks  high  among  the  causes  of  chronic  abdominal  distress. 
Numerically  in  my  index  it  is  more  frequent  than  gastric 
ulcer,  but  less  frequent  than  duodenal  ulcer,  conditions 
which  are  far  more  likely  to  be  referred  for  a second  opinion. 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  170 


Nature  of  toe  Disorder 

‘Spastic  colon*  falls  into  the  category  of  the  visceral 
neuroses.  Its  association  with  certain  physical  and  psycho- 
logical  types;  its  intermittent  behaviour;  its  aggravation 
by  circumstances  which  depress  or  harass  the  higher  centres, 
and  the  absence  of  all  evidence  of  an  associated  organic 
lesion,  give  credence  to  this  view.  It  is  a close  ally  to  bron- 
chial asthma,  in  which  an  inherited  irritability  of  the  bron- 
chial centres  and  a sensitiveness  to  certain  local,  psychic, 
and  peripheral  stimuli  are,  on  Hurst’s  [0]  showing,  so  appar- 
ent. Just  as  with  asthma,  so  with  spastic  colon,  cases  occur 
in  which  spasm  alone  is  the  outstanding  feature,  and  others 
in  which  mucorrhoca  is  supcradded.  Asthma  is  sometimes 
coincident  with  colonic  spasm  in  the  same  patient  or  re- 
corded in  n near  relative.  The  stimuli  which  may  provoke 
and  perpetuate  an  attack  of  colonic  spasm  include  (1)  local 
stimuli  (coarse  foods,  purgatives,  constipation),  (2)  central 
nervous  stimuli  (worry),  (8)  external  peripheral  stimuli 
(cold).  The  same  irritability  of  plain  muscle  is  often  simul- 
taneously manifest  as  bladder  frequency  and  even  bladder 
pain,  especially  in  female  sufferers  from  spastic  colon;  in 
pyloric  spasm;  spasmodic  dysmenorrhoea ; and  in  the 
vascular  spasm  which  gives  rise  to  ‘dead  fingers’. 

Nature  or  toe  Spasm  and  Pain 

In  obstructive  or  irritative  lesions  of  the  colon  there  is 
increased  peristaltic  activity  with  more  or  less  rhythmical 
griping  due  to  the  passage  of  waves  of  contraction  involv- 
ing successive  groups  of  circular  fibres.  In  spastic  colon  no 
such  rhythmical  movements  are  provoked,  but  the  tonus  or 
posture  of  the  muscle-fibres,  including  the  longitudinal 
fibres,  is  modified  in  such  a way  as  to  impart  a sustained 
shortening,  with  rigidity  and  narrowing  of  the  lumen,  to 
portions  of  the  bowel  wall  often  many  inches  in  extent. 
The  hardness  and  equally  the  straightening  and  shortening 
of  the  affected  loop  cannot  be  otherwise  explained.  I was  at 
one  time  puzzled  by  finding  a hardened  and  horizontal 
transverse  colon  crossing  the  epigastrium,  for  although  this 


180  CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON 
is  its  anatomical  situation  I knew  that  the  radiologist  more 
frequently  showed  this  structure  as  a festoon  in  the  middle 
or  lower  abdominal  planes  and  sometimes  even  in  the  true 
pelvis.  Surgeons  sometimes  witness  the  phenomenon  of 
tonic  hardening  in  the  course  of  a laparotomy  when  the 
affected  loop  becomes  rigid,  pale,  and  erect  in  the  wound. 
I know  no  clinical  condition  which  better  supports  the 
hypothesis  that  visceral  pain  originates  in  the  viscus  and  is 
due  to  increased  tension  in  the  muscle-fibre  than  spastic 
colon.  With  no  inflammatory  disease  to  involve  the  other 
coats  of  the  bowel  or  neighbouring  tissues,  and  so  to  confuse 
the  issue,  it  is  possible  to  demonstrate  in  these  cases  at  once 
a complete  absence  of  somatic  hyperalgesia  and  well-defined 
pain  and  tenderness  in  the  affected  bowel  itself,  a pain  and 
tenderness  which  increase  when  the  hardening  increases  and 
diminish  when  it  diminishes.  The  sustained  and  aching 
character  of  the  pain  accords  well  with  this  durable  modifica- 
tion of  tonus  or  posture,  and  contrasts  with  the  sharper, 
transient  agony  of  peristaltic  colic. 

Illustrative  Cases 

Case  2.  Illustrating  the  influence  of  cold,  the  simulation  of  appendi- 
citis, and  the  cause  of  the  pain. — A young  and  athletic  lady,  aged  25, 
developed  pain  in  the  right  iliac  fossa  on  a long  voyage.  The  ship’s 
doctor  diagnosed  appendicitis,  but  would  not  operate  on  board.  On 
arrival  in  England  her  own  medical  adviser  and  a surgeon  saw  her 
and  concurred  in  the  diagnosis,  but  freely  admitted  that  the  appendix 
when  removed  was  ‘disappointing*.  The  other  organs  were  healthy. 
The  pains  recurred  and  she  was  brought  to  see  me.  I obtained  an 
earlier  history  of  many  attacks  of  sudden  and  intensely  severe  pain 
coming  on  ten  minutes  after  a long  surim,  in  which  she  was  doubled  up, 
looked  green  and  ill,  but  was  relieved  by  brandy.  Since  the  operation 
there  had  been  a slight  looseness  of  the  bowels.  She  had  noticed 
aggravation  by  fatigue,  cold,  and  by  fruit  and  green  vegetables. 
During  my  examination  I was  able  to  demonstrate  a hardening  of  the 
colon  in  the  right  Iliac  fossa  which  came  and  went,  the  pain  coming 
with  the  ‘lump*  and  disappearing  as  it  ‘faded’.  The  diagnosis  had 
been  made  easier  for  me  by  the  negative  operation  findings,  but  the 
earlier  history  of  precipitation  by  cold  was  instructive. 

Case  3.  Illustrating  difficulties  in  differential  diagnosis,  the  occa- 
sional severity  of  the  pain,  and  aggravation  by  an  enema,  jolting,  d-c. — 
An  infantry  officer,  aged  41,  consulted  me  on  25  February  1026  for 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  181 
severe  pain  in  the  left  subcostal  region  passing  through  to  the  back 
at  the  same  level.  He  had  also  felt  the  pain  in  the  mid-epigastrium 
where  he  had  been  tender.  He  had  suffered  similar  symptoms  a year 
and  also  5 months  previously,  but  less  severely.  The  pain  was  liable 
to  come  one  or  two  hours  after  food,  and  was  sometimes  relieved  by 
eating.  Jolting  dellnitoly  aggravated  it.  His  actual  sensations  he 
likened  to  *a  lump  of  dough  stuck  and  swelling  as  though  about  to 
burst*.  He  was  lean,  tense  and  tremulous,  and  very  tender  in  mid- 
epigastrium.  I made  a provisional  diagnosis  of  gastric  ulcer  and  put 
Itim  into  a nursing  home  For  observation.  On  27  February  he  had  a 
very  severe  attack  of  pain  below  the  left  rib  margin  and  radiating 
down  towards  the  groin.  The  pain  immediately  followed  an  enema. 
Morphine  was  given  on  more  than  one  occasion.  He  was  tender  under 
the  left  ribs  and  3 queried  feeling  the  kidney.  Jarring  the  loin  also 
caused  pain.  Urine  normal.  His  wife  then  remembered  that  for  years 
he  had  had  an  occasional  day  in  bed  for  left-sided  pain.  While  I was 
away  for  a week-end,  the  patient,  roy  deputy,  and  the  nurses  all 
noted  the  presence  of  a lump  below  the  ribs  which  was  gone  on  my 
return.  I now  decided  to  regard  the  symptoms  as  renal.  A surgical 
colleague  who  saw  1dm  with  me  concurred,  but  cystoscopy  and  pye- 
lography were  negative.  The  pain  continued,  and  he  was  explored  on 
14  March,  nil  investigations  having  proved  negative  and  all  medical 
treatment  unavailing.  A slightly  fibrotic  appendix  was  removed,  and 
adhesions  between  the  duodenum  and  gall-bladder  were  freed.  No 
ulcer,  gall-stones,  growth,  or  other  abnormality  were  demonstrable. 
He  was  not  relieved  of  Ids  symptoms  by  the  operation,  although  re- 
assured in  his  mind  by  the  findings.  I was  then  able  to  satisfy  myself 
that  both  the  pain  and  the  lump  were  colonic  and  due  to  tonic  con- 
traction. I have  seen  only  a few  other  coses  in  which  the  pain  was  so 
severe  and  none  so  deceptive  in  their  symptomatic  associations.  I saw 
this  patient,  who  remains  on  duty,  later,  and  was  able  to  feel  the 
hardened  colon  to  the  left  of  the  navel.  He  is  quite  sure  that  jolting 
and  cold,  which  I had  come  in  the  interval  to  recognize  in  other  cases 
ns  important  aggravating  factors,  are  very  definitely  so  in  his  case. 
I should  clearly  have  paid  more  attention  in  his  first  bad  attack  to 
the  influence  of  the  enema. 

Case  4.  Illustrating  the  severity  of  symptoms,  ballooning  of  the  caecum 
the  shortening  and  straightening  of  the  colon,  and  the  accuracy  of  localiza- 
tion by  the  patient's  gesture. — I was  consulted  by  a woman  aged  40. 
From  girlhood  she  had  suffered  from  constipation  and  n liability  to 
nausea,  and  had  been  prevented  by  her  poor  health  from  taking  up 
work  in  which  she  was  interested.  In  2021  she  had  acute  gangrenous 
appendicitis.  Since  then  she  had,  in  the  words  of  her  medical  adviser, 
had  three  or  four  attacks  ‘almost  like  partial  obstruction*.  These 
start  with  feelings  of  pain  and  weight  in  the  caecal  region  where  a big 
bulge  appears.  In  her  last  attack  she  could  ‘feel  the  bowel  like  a 


182  CHRONIC  SPASMODIC  AFFECTION’S  OF  THE  COLON 
lump  \ and  was  in  pain  for  four  or  five  hours  continuously.  The  pain 
also  passed  straight  across  her  abdomen  to  the  left.  Lesser  attacks 
were  brought  on  by  work  in  the  garden  and  could  be  cut  short  by 
lying  down.  There  was  aggravation  by  purgatives  and  her  pain  was 
worse  after  dcfnecation.  On  palpation  I was  able  to  feel  a hardened 
colon  which  again  ‘faded’  under  my  hand.  The  radiograms  showed 
an  extreme  degree  of  colonic  spasm  affecting  first  the  transverse  and 
later  the  descending  portion.  During  the  examination  slic  surprised 
the  radiologist  by  accurately  tracing  the  course  of  the  transverse  colon 
by  her  sensations.  This  straight  course  from  hepatic  to  splenic  flexure 
is  well  shown  in  the  illustrations  to  Lecture  XI.  Her  brother  later 
consulted  me  for  similar  symptoms. 

Treatment 

Most  patients  with  ‘spastic  colon’  have  been  walking  in 
fear  of  organic  disease ; many  of  them  have  been  told  that 
they  have  organic  disease;  cancer-phobia  is  frequently  pre- 
sent; operations  may  have  been  advised  or  already  per- 
formed. The  first  duty  of  the  physician  is  therefore  full 
reassurance.  With  this  must  be  combined  a simple  explana- 
tion of  the  nature  of  the  disorder  and  the  mode  of  origin  of 
the  pain.  Under  general  hygienic  measures  the  importance 
of  mental  and  physical  relaxation,  of  holidays,  of  moderate 
exercise,  of  warmth,  and  a sensible  mixed  diet  must  be 
enumerated.  Often  the  diet  has  been  cut  too  low  and  fruit 
and  vegetables  have  been  too  rigorously  excluded.  The 
bulky  starchy  foods,  potatoes,  beans,  and  peas,  which  pre- 
dispose to  intestinal  flatulence,  are  better  avoided,  but  fruits 
of  all  kinds,  excepting  those  with  tough  skins  and  seeds,  and 
the  softer  green  vegetables  should  be  liberally  prescribed 
together  with  whole-meal  bread  and  farm  produce  as  a 
natural  treatment  of  the  costive  tendency.  Tobacco  may 
require  restriction  or  even  be  forbidden  for  a long  test- 
period.  Purgatives  must  be  entirely  forbidden,  but  lubri- 
cants may  be  given.  Belladonna  in  full  pharmacopoeial 
doses  helps  to  relax  the  spasm.  Bromides  should  be  reserved 
for  the  anxious  and  ‘jumpy’  patients,  and  witliheld  in  the 
case  of  the  more  jaded  and  depressed.  There  is  commonly 
restlessness  with  a furrowed  brow,  and  hypertonus  of  skele- 
tal muscles.  Psychotherapy  plays  an  important  part  in  the 
treatment  of  such  cases.  Jackson  [10]  has  described  a 


CHRONIC  SPASMODIC  AFFECTIONS  OF  THE  COLON  183 
method  of  treatment  by  ‘progressive  relaxation’  in  ivhieh 
clinical  improvement  is  shown  to  coincide  with  a return  to 
normal  in  the  colonic  radiograms  and  diminution  in  the 
briskness  of  the  knee-jerks.  The  good  sleep  enjoyed  by 
most  patients,  even  when  suffering  bad  pain  by  day,  is  prob- 
ably due  to  the  relief  afforded  by  natural  muscular  repose. 
In  some  cases  the  sallow  complexion  and  lassitude  and  a 
furred  tongue  during  the  attacks  seem  to  suggest  an  element 
of  what — for  want  of  a more  precise  term — we  must  con- 
tinue to  refer  to  as  intestinal  toxaemia.  I think  it  must  be 
in  these  cases  especially  that  Stacey  Wilson  obtains  his 
successes  by  exhibiting  liquor  hydrarg.  perchlor.  with  liquor 
ferri  perchlor.  I have  not  tried  his  prescription  extensively, 
but  in  one  case  it  seemed  to  bring  about  a remarkable  im- 
provement when  other  remedies  had  failed  and  the  patient 
was  begging  for  an  exploration.  In  cases  with  severe  pain 
and  in  exacerbations  of  mucous  colic,  initial  large  warm 
enemata  administered  very  slowly,  both  to  give  lavage  and 
to  overcome  the  spasm,  and  rectal  injections  of  warm  liquid 
paraffin  (4  or  5 oz.)  to  be  retained  overnight,  are  useful.  The 
disorder,  being  like  asthma  and  migraine,  so  largely  depen- 
dent on  constitutional  factors,  is  difficult  to  ‘cure’,  but 
repeated  reassurances  and  rational  treatment  will  often 
mitigate  symptoms  even  in  bad  cases.  In  milder  cases  there 
may  be  complete  relief. 

Conclusion 

I have  attempted  a somewhat  detailed  analysis  of  the 
clinical  picture  of  spastic  colon  because  the  diagnosis  of  the 
condition  should  generally  be  possible  on  clinical  grounds. 
Furthermore  in  functional  disorders  of  this  kind  special 
investigations  inevitably  give  a high  percentage  of  negative 
results.  The  recognition  of  spastic  colon  as  an  occasional 
cause  of  very  severe  abdominal  pain  and  as  a common  cause 
of  persisting  or  recurring  pain  in  the  right  iliac  fossa  is,  I 
believe,  especially  worthy  of  emphasis.  Writing  of  these 
visceral  neuroses  in  1906  Hawkins  said,  ‘They  are  at  this 
moment  particularly  worthy  of  study,  owing  to  the  advance 
of  abdominal  surge ry,  not  because  they  are  amenable  to 


1 84  CHRONIC  SPASMODIC  AFFECTIONS  OF  TIIE  COLON 
surgical  treatment,  but  rather  because  they  need  protec- 
tion.’ I think  it  should  be  accepted  that  they  still  need 
protection,  and  that  for  this  and  other  reasons  they  are  still 
worthy  of  study. 


REFERENCES 

1.  IIuasT,  A.  F.:  Constipation  and  Allied  Intestinal  Disorders. 

London,  1010. 

2.  Ilowsmr,  J.:  Practical  Itemarks  on  the  Discrimination  and  Suc- 

cessful Treatment  of  Spasmodic  Stricture  in  the  Colon.  London, 
1830. 

3.  CitEncnawsKY:  Ilev.  de  Mid.,  18S3,  iii.  876  and  1033. 

4.  FleineB,  IV’.:  Deri.  Win.  IPodt.,  1893,  xxx.  CO  and  03. 

5.  Hawkins,  II.  P.:  Brit.  Med.  Joum.,  100C,  i.  05. 

0.  TurnEB,  P.:  Guij's  IIosp.  Pep.,  102-1,  bcriv.  55. 

7.  StaceV  VVitsON,  T. : Brit.  Med.  Joum.,  1022,  i.  041. 

8.  Tonic  Hardening  of  the  Colon.  London,  1027. 

0.  IIuhst,  A.  F.:  Medical  Essays  and  Addresses.  London,  1024. 

10.  Jackson,  E.:  Arch,  of  Internal  Med.,  1027,  scxxix.  433. 


XIII 

ON  EXAMINING  THE  RECTUM1 
Tiie  end  of  the  alimentary  passage  hides  many  secrets 
which  are,  in  more  senses  than  one,  fundamental,  for  dia- 
gnosis and  appropriate  treatment  depend  upon  their  timely 
discovery.  There  is  a saying  that  the  chief  clinical  advan- 
tage of  the  consultant  over  the  general  practitioner  lies  in 
his  more  frequent  appreciation  of  the  necessity  for  a rectal 
examination.  This  might  seem  to  suggest  errors  of  omission 
on  the  part  of  colleagues,  but  it  is  not  a general  criticism, 
and  it  might  equally  be  taken  as  a reflection  on  teaching. 
AU  doctors  in  all  branches  of  the  profession — and  consul- 
tants are  no  exception — are  guilty  of  omissions  from  time 
to  time,  for  they  are  only  human,  but  the  best  doctors 
include  those  who  can  claim  the  fewest  omissions  in  respect 
of  this  simple  procedure. 

I have  recently  looked  through  my  notes  of  14  cases  of 
carcinoma  of  the  rectum.  These  cases  do  not  usually  find 
their  way  to  the  physician;  they  go  to  the  surgeon,  and  the 
majority  presumably  go  with  the  diagnosis  already  made. 
Of  these  14  cases,  however,  8 had  not  been  diagnosed,  not- 
withstanding that  they  had  had  characteristic  symptoms 
for  periods  varying  from  three  months  to  four  years.  Seven 
had  never  had  the  rectum  examined.  Five  had  symptoms 
dating  back  over  a year,  and  2 over  three  years.  The  usual 
diagnosis  in  unexamined  cases  teas  ‘ colitis' . 

This  important  procedure  is  apt  to  be  neglected  (1) 
through  lack  of  appreciation  of  the  indications,  and  (2) 
through  a natural  sense  of  delicacy  in  regard  to  an  examina- 
tion which,  in  the  idea,  is  so  unpleasant  and  so  likely  to  be 
repugnant  to  the  patient.  Some  patients  who  have  to 
submit  to  it  are,  in  point  of  fact,  most  considerate,  and  will 
even  express  sympathy  for  the  doctor  that  such  a duty 
should  fall  to  him.  Others  are  squeamish  or  timid,  but  if 
we  make  a point  of  being  gentle,  and  are  careful  to  explain 
1 Guy'*  Hasp.  Gazelle,  1031,  xlv.  122. 


180  ON  EXAMINING  THE  RECTUM 

the  value  of  the  examination  and  how  quickly  it  is  over, 
and  to  warn  them  that,  while  it  is  likely  to  be  uncomfortable 
it  is  only  occasionally  painful,  confidence  can  soon  be  won. 

A decision  to  make  the  examination  must  obviously  be 
based  on  history  and  symptoms.  It  would  clearly  be  an 
excess  of  zeal  to  make  it  a part  of  every’  routine  overhaul. 
The  behaviour  of  the  bowel,  abnormalities  in  the  consis- 
tence and  appearance  of  the  stools,  and  local  pain  or  dis- 
comfort are,  of  course,  the  chief  indications.  If  blood  is 
passed  it  should  be  particularly  noted  whether  this  is  with 
a formed  or  unformed  stool,  whether  it  comes  with  the  stool 
or  separately  at  the  end  of  it,  and  so  forth.  The  diseases 
which  we  set  out  to  diagnose  with  the  help  of  the  examina- 
tion arc  chiefly  situated  in  the  ano-rectal  canal  or  its  near 
neighbourhood,  but  they  may  also  be  remotely  removed 
from  it. 

The  Indications  for  a Rectal  Examination 

The  principal  symptoms  and  occasions  which  call  for  the 
examination  are: 

1.  Pain  in  the  anal  or  rectal  canal;  bleeding  from  the 
rectum ; passage  of  mucus  or  pus  from  the  rectum ; chronic 
diarrhoea;  obstinate  constipation;  alternating  constipation 
and  diarrhoea;  anal  pruritus — symptoms,  in  other  words, 
suggestive  of  carcinoma,  fistula,  fissure,  piles,  proctitis,  or 
colitis.  Rectal  prolapse  or  symptoms  of  intussusception  in 
children  are  further  obvious  indications. 

2.  Urinary  symptoms  suggesting  enlargement  of  the  pros- 
tate or  pressure  upon  the  bladder  or  symptoms  of  disease 
of  the  genito-urinary  apparatus  which  might  involve  the 
seminal  vesicles  in  the  male. 

3.  Symptoms  of  uterine,  ovarian,  or  tubal  disease  in  the 
female  and  particularly  in  unmarried  women  when  a vaginal 
examination  is  to  be  avoided. 

4.  Any  suspicion  of  serious  abdominal  disease,  inflam- 
matory or  malignant,  in  which  the  possibility  of  feeling  an 
inflammatory  mass  (as  in  appendicitis)  or  deposits  of  new 
growth  (as  in  carcinoma  of  the  stomach  or  bowel)  is  enter- 
tained. 


ON  EXAMINING  THE  RECTUM  187 

5,  Sciatic  or  hip  pain  or  other  symptoms  of  possible  bony 
disease  involving  the  sacrum  or  pelvis,  and  including  osteo- 
myelitis, tubercular  trouble,  and  bony  tumours. 

0.  Rectal  spasms,  and  crises  of  nervous  origin  where  we 
must,  nevertheless,  be  at  pains  to  exclude  a local  cause. 

7.  Severe  unexplained  anaemia  where  malignant  disease, 
a local  source  of  venous  or  arterial  bleeding,  or  a tarry  smear 
on  the  tip  of  the  finger-stall  may  give  the  answer  to  our 
question. 

8.  Obscure  pyrexia  in  cases  where  it  has  become  neces- 
sary to  exclude  local  inflammatory  or  malignant  causes. 

This  is  a sufficiently  long  list,  but  not  exhaustive. 

The  Technique 

The  anus  and  rectum  may  be  examined  (a)  with  the  fore- 
finger, (6)  with  the  anal  speculum,  (c)  with  the  proctoscope 
or  sigmoidoscope,  and  (d)  by  direct  inspection  during  dilata- 
tion of  the  sphincter  under  an  anaesthetic.  The  most  im- 
portant is  the  digital  method,  but  more  accurate  informa- 
tion is  often  obtained  by  one  of  the  visual  methods.  Some 
teachers,  I believe,  advise  that  finger-stalls  should  not  be 
used,  as  they  diminish  tactile  accuracy.  You  should  certainly 
never  employ  the  thicker  finger-stalls  provided ; the  finger 
of  an  ordinary  rubber  operating-glove  is  generally  too  thick. 
The  thin  ‘film’  finger-stalls,  however,  now  on  the  market 
are,  to  my  mind,  satisfactory.  They  are  more  hygienic  than 
the  naked  finger,  and  they  afford  protection  against  an 
occasional,  but  ever  possible,  risk  of  infection.  I have  never 
regretted  my  custom  of  using  one  since  I examined  a case 
of  undiagnosed  anal  soreness  in  a young  man,  who  in  the 
following  week  developed  a profuse  syphilitic  rash.  Condylo- 
mata  are  among  the  most  infective  of  syphilitic  lesions. 

The  Digital  Method 

For  this  examination  the  patient  is  placed  in  the  left 
lateral  position ; the  knees  should  be  well  drawn  up  towards 
the  chest,  with  the  buttocks  on  a level  with  or  just  over  the 
edge  of  the  bed  or  couch.  The  anal  orifice  should  first  be 


183  ON  EXAMINING  THE  RECTUM 

inspected  for  external  piles  or  for  the  surrounding  sodden 
skin  of  pruritus  ani,  and  then  anointed  with  vaseline.  Care 
should  be  taken  to  avoid  introducing  hair  with  the  finger. 
Then,  if  the  finger  is  inserted  gently  and  slowly,  discomfort 
will  be  reduced  to  a minimum.  The  examination  may  be 
excessively  painful  in  the  presence  of  fistula,  fissure,  a 
thrombosed  pile,  a low  rectal  carcinoma,  in  cases  of  faecal 
impaction,  and  in  certain  cases  of  anal  spasm.  Otherwise 
it  is  usually  only  uncomfortable.  It  commonly  evokes  a 
sense  of  the  desire  to  defaecate,  and  is  therefore  a cause  of 
mental  distress,  which  can  easily  be  explained  away.  . 

What  are  the  abnormalities  which  the  finger  may  en- 
counter ? Piles,  unless  they  have  recently  been  thrombosed, 
are  soft  structures  and  seldom  very  evident.  An  anal  fissure, 
or  more  correctly  an  anal  ulcer  (the  impression  of  a crack  or 
fissure  is  due  to  the  fact  that  the  ulcer  is  laterally  com- 
pressed by  the  postural  tone  of  the  sphincter),  may,  for  all 
its  minuteness,  give  a very  definite  impression  to  the  finger- 
tip, and  this  is  best  likened  to  the  feeling  of  the  button-hole 
on  the  lapel  of  one’s  coat.  The  track  of  a small  peri-anal 
fistula  or  abscess  may  be  felt  as  a small  linear  prominence. 
Direct  pressure  upon  an  ulcer  or  an  abscess  nearly  always 
evokes  instant  pain.  Ballooning  of  the  rectum  gives  the 
impression  of  a large  hollow  cavern  when  the  finger  lias 
passed  beyond  the  sphincter.  By  some  tliis  is  thought  to  be 
a sign  of  obstruction  higher  up.  This  is  not  necessarily  so, 
but  it  is  more  common  in  obstructions  or  other  chronic 
bowel  diseases  than  in  their  absence.  A carcinoma  may  be 
felt  ns  the  elevated  edge  of  a hard  ulcer  over  which  the 
finger-tip  rides  before  it  drops  into  a roughened  crater,  or  as 
an  irregular  tumour  filling  the  lumen  of  the  bowel.  Scybala 
in  a neighbouring  loop  may  easily  be  mistaken  for  a tumour 
or  glands.  Retained  faeces  may  be  present  in  the  rectum  as 
a soft  mass  or  scybalous  lumps,  or,  occasionally,  as  a large 
impacted  mass  capable  of  causing  severe  symptoms,  as  I 
shall  describe. 

In  certain  cases  it  may  be  necessary'  to  make  a bi-manual 
examination.  It  is  then  wiser  to  roll  the  patient  on  to  Iiis 
back,  keeping  the  finger  in  position  meanwhile,  when  gentle 


ON  EXAMINING  THE  RECTUM  189 

pressure  on  the  abdomen  may  bring  a tumour,  which  could 
not  otherwise  be  felt,  in  contact  with  the  finger-tip. 

On  withdrawing  the  finger,  which  should  be  done  slowly 
and  gently,  the  finger-stall  should  be  inspected  for  blood  or 
pus,  or  to  observe  the  colour  of  adherent  faecal  matter. 

Instrumental  Methods 

First,  we  have  the  anal  speculum  originally  devised  by 
Hilton,  which  is  most  useful  for  inspecting  and  giving  access 
to  an  anal  ulcer.  The  instrument  explains  itself;  the  re- 
moval of  the  lateral  slide  gives  a clear  view  of  the  diseased 
area. 

For  the  proctoscope  and  sigmoidoscope  we  employ  the 
same  technique,  and  they  may  be  considered  together. 
With  regard  to  the  preparation  of  the  patient,  no  purgation 
should  be  used.  If  he  is  up  and  about  he  should  be  encour- 
aged to  have  the  bowel  moved  an  hour  before  the  examina- 
tion. If  confined  to  bed,  a warm  water  wash-out  should  be 
given  early  on  the  morning  of  the  examination,  and  a later 
attempt  at  natural  evacuation  should  be  encouraged.  A 
nervous  patient  may  be  given  a morphine  injection  20 
minutes  before  the  examination,  and  if  there  is  anal  soreness 
a cocaine  suppository  may  be  inserted.  Unless  the  general 
condition  prohibits  it,  the  examination  should  be  made 
without  an  anaesthetic,  in  the  knee-elbow  position,  with 
the  shoulders  low  and  the  buttocks  raised  and  the  back  well 
hollowed.  Before  the  instrument  is  passed  a digital  examina- 
tion should  be  made  (1)  to  afford  a reminder  of  the  direction 
taken  by  the  anal  canal  and  the  angle  which  it  forms  with 
the  rectum,  and  (2)  because  it  effects  a slight  preliminary 
dilatation  before  the  bigger  instrument  is  inserted.  As 
soon  as  the  instrument  has  been  passed  within  the  rectum 
the  plunger  should  be  removed  and  the  light  inserted,  and 
all  further  progress  in  its  passage  should  thereafter  be 
guided  by  sight.  The  normal  landmarks  are  the  two 
Houston’s  folds,  rather  reminiscent,  when  viewed  simul- 
taneously, of  the  diaphragm  of  a camera -shutter,  and  beyond 
these  the  pelvi-rectal  flexure.  As  careful  an  inspection 
should  be  made  in  withdrawing  the  instrument  as  in  passing 


100  ON  EXAMINING  THE  RECTUM 

it.  Only  during  withdrawal  can  we  observe  the  state  of  the 
anal  canal.  The  colour  and  smoothness  or  otherwise  of  the 
rectal  mucosa,  bleeding  on  contact  with  the  instrument,  or 
blood,  mucus,  or  pus  coming  down  from  above  should  all  be 
looked  for,  as  well  as  surface  ulcerations  or  grosser  lesions. 

Let  us  now  pass  to  a review  of  some  illustrative  cases. 

Carcinoma  of  Vie  Rectum 

Case  1.  A woman,  aged  58,  coming  from  abroad,  stated  that  she 
had  had  an  operation  for  removal  of  her  appendix  4 years  previously. 
The  pain  for  which  the  operation  was  performed  persisted  afterwards. 
Two  years  later  she  had  the  first  of  a series  of  violent  attacks  of  lower 
abdominal  colic.  For  18  months  she  had  had  continuous  abdominal 
discomfort  and  pain,  and  during  the  past  10  months  had  frequent 
calls  to  stool  with  passage  of  blood  and  mucus.  She  had  lost  3 stone 
in  weight  during  4 years,  was  emaciated  and  cachectic.  She  had 
been  treated  for  ‘colitis*,  and  the  stools  had  been  examined  baeterio- 
logically  to  exclude  dysentery.  Rectal  examination  showed  the  pelvis 
filled  with  a hard  mass,  and  also  a hard  villous  tumour  filling  the 
lumen  of  the  bowel.  Probably  the  growth  had  been  there  for  at  least 
2 years,  and  possibly  the  pain  for  which  the  nppendiccctomy  had 
been  performed  4 years  previously  was  the  first  manifestation. 

Case  2.  A woman,  aged  61,  was  sent  to  me  with  a diagnosis  of 
mucous  colitis.  She  had  been  seen  by  more  than  one  doctor  in  her 
own  town,  had  been  sent  to  Leamington  for  special  treatment  nnd 
was  there  examined  radiologically,  and  had  had  Plombiircs  treat- 
ment at  Harrogate.  The  duration  of  her  illness  was  3 years.  The 
symptoms  had  started  abruptly  in  the  first  instance  with  the  passage 
of  blood  and  mucus,  and  frequent  calls  to  stool.  She  had  gradually 
become  worse,  and  her  complaint  was  of  violent  pain  in  the  lower 
abdomen  and  a sensation  ‘as  though  her  intestine  was  trying  to  pass 
out  by  the  bowel*.  Frequency  and  urgency  were  so  pronounced  as 
to  necessitate  taking  a bed-pan  to  bed.  She  had  lost  over  a stone  and 
was  thin  and  anaemic.  At  the  limit  of  the  finger  a hard  ulcer  with 
a well-defined  edge  and  rough  base  could  be  felt. 

In  such  cases,  even  if  rectal  examination  at  an  earlier 
stage  failed  to  make  the  diagnosis,  the  symptoms  called  for 
r proctoscopic  or  sigmoidoscopic  examination.  Bacterio- 
logical and  X-ray  examinations  are  clearly  quite  out  of  place 
until  the  bozeel  has  been  examined  both  digitally  and  visually. 

Anal  Ulcer 

Case  3.  A woman,  aged  40,  was  sent  into  hospital  under  my  care 
in  November  1 927  for  recurring  haemorrhage  from  the  bowel  and  pro- 


ON  EXAMINING  THE  RECTUM  101 

found  anaemia.  The  first  haemorrhage  had  been  noticed  in  1913,  and 
she  was  treated  for  bleeding  piles.  This  diagnosis  was  confirmed  by 
another  doctor  in  1015.  The  bleeding  would  last  for  a few  days,  and 
then  recur  again  after  o few  months.  Gradually  the  attacks  became 
more  frequent.  In  1920  she  was  sigmoidoscopcd  and  a small  polyp 
was  removed,  but  without  any  effect  upon  her  symptoms.  In  3027 
the  haemorrhages  became  still  more  frequent.  She  became  weak  and 
anaemic  and  complained  of  shortness  of  breath.  Haemoglobin  on 
admission  was  47  per  cent.  I examined  her  with  the  sigmoidoscope 
on  28  November  1927,  passing  the  instrument  10  in.  without  diffi- 
culty. No  abnormality  was  noted  excepting  a vascular  mucosa  in 
the  anal  canal.  No  bleeding  occurred  at  the  time.  As  no  cause  for 
the  haemorrhage  had  been  forthcoming  I examined  her  again  with 
the  sigmoidoscope  on  13  December,  with  a negative  result,  and  then 
repeated  the  digital  examination  and  felt  a small  posterior  anal 
ulcer.  Pressure  upon  this  caused  distinct  pain.  On  re-interrogation 
it  now  became  clear  that  the  stools  were  usually  passed  separately 
and  that  bright  blood  followed.  For  the  first  time  the  patient  ad- 
mitted also  to  a ‘bearing  down*  pain  after  defaccation.  She  was  next 
examined  by  Mr.  E.  C.  Hughes  under  an  anaesthetic,  when  a small 
posterior  anal  ulcer  with  a spouting  arteriole  in  its  base  was  found 
and  cauterized.  General  advice  about  keeping  the  stools  soft  was 
given,  and  the  patient’s  doctor  reported  in  March  of  the  next  year 
that  there  had  been  no  further  bleeding  and  that  the  patient  felt 
better  than  for  many  years. 

Here,  then,  was  a case  of  intermittent  ill  health  dating 
from  1913  to  1927,  with  severe  anaemia  latterly,  due  to  a 
lesion  so  minute  that  it  had  several  times  escaped  detection 
at  various  hands.  A digital  examination  and  a more  careful 
analysis  of  the  symptoms  suggested  a diagnosis  which  direct 
inspection  proved. 

Here  is  a second  case  of  anal  ulcer  but  with  different 
symptoms. 

Case  4.  A woman,  aged  33,  was  sent  to  me  with  an  18-montlis’ 
history  of  pain,  feeling  to  the  patient  Tike  a fragment  of  china  stuck 
somewhere  low  down'  in  the  left  iliac  fossa  just  above  tiie  groin, 
passing  to  a similar  point  in  the  hack  and  spreading  out  into  the  left 
hip.  Her  doctor  favoured  a diagnosis  of  ureteric  calculus.  I dis- 
covered from  her  that  the  pain  was  aggravated  by  cold  and  by 
jolting  in  a motor-car,  that  the  bowels  were  costive,  that  for  a much 
longer  period  than  18  months  she  had  frequently  passed  a little  blood 
at  the  end  of  defaecation,  and  that  defaecation  had  also  been  painful. 
I found  no  evidence  of  disease  until  I came  to  the  Tectal  examination. 


102  ON  EXAMINING  THE  HECTUM 

This  caused  undue  pain,  and  revealed  a tender  point  corresponding 

with  a small,  roughened  area  typical  of  final  ulcer. 

Those  of  you  who  are  not  already  familiar  with  them 
should  read  in  Hilton’s  Best  and  Pain  his  descriptions  of  cases 
of  anal  ulcer  with  misleading  secondary  symptoms  and 
referred  pains,  and  particularly  the  case  of  the  bright  young 
lady  in  society  whose  abdomen  became  swollen,  whose 
character  suffered  a striking  change,  who  was  suspected  by 
one  doctor  of  pregnancy,  who  became  anaemic  and  endured 
much  distress  of  body  and  mind,  but  whose  symptoms  were 
all  eventually  shown  to  be  due  to  a small,  painful  anal  ulcer. 

If  I were  to  attempt  a clinical  lecture  on  ‘ Minor  Maladies 
with  Major  Symptoms’  I should  head  the  list  with  anal 
ulcer. 

Ischio-recial  Abscess 

I was  asked  to  see  a man  who  had  been  troubled  for  three 
years  by  the  most  wearing  pain  felt  over  the  sacrum,  and 
occasionally  radiating  along  the  course  of  the  right  sciatic 
nerve.  He  had  never  passed  blood,  but  occasionally  there 
was  a little  watery  discharge  after  the  motion.  His  doctors 
had  examined  the  bowel  on  many  occasions,  but  had  found 
no  cause.  The  sphincter  had  been  stretched  twice,  with  only 
transient  relief.  They  had  been  forced  to  the  conclusion 
that  the  patient  was  a neurasthenic,  but  without  feeling 
satisfied  that  there  was  no  local  physical  basis.  Close  in- 
quiry elicited  the  fact  that  the  pain,  although  temporarily 
easier,  was  later  worse  after  defaecation.  I was  lucky,  for  on 
rectal  examination  I found  on  the  right  side  at  the  limit  of 
the  finger  a small  linear  ridge.  Pressure  upon  this  caused 
pain,  and  also  produced  a flow  of  pus  down  the  side  of  my 
finger  amounting  to  half  a drachm.  It  was  clear  that  he  had 
a small  peri-anal  or  ischio-rectal  abscess,  which  underwent 
spontaneous  evacuation  from  time  to  time. 

Ball-valve  Accumulations  in  the  Bectum1 

Occasionally  debilitated  patients,  and  particularly  the 
more  elderly,  will  accumulate  large  masses  of  faecal  matter 

* See  also  Lecture  XIV. 


ON  EXAMINING  THE  RECTUM  103 

in  the  rectum  which  they  cannot  expel.  This  is  especially 
likely  to  occur  after  any  kind  of  dehydration,  after  a gastric 
haemorrhage,  or  after  a barium  meal. 

Case  5.  A woman,  aged  72,  consulted  me  on  30  June  1032.  From 
September  1031,  when  her  symptoms  started  quite  abruptly,  she  h3d 
been  troubled  with  great  bowel  discomfort.  There  were  four  or  live 
calls  to  stool  each  day,  sometimes  with  a loose  result,  sometimes  with 
none,  and,  in  the  latter  event,  there  was  much  rectal  pain.  Mucus 
had  been  noticed,  but  blood  on  one  occasion  only.  Visits  had  been 
made  to  an  institution  where  'expert'  boweMavagc  was  given  but 
without  the  slightest  benefit.  The  weight  had  dropped  half  a stone. 
The  patient  was  of  robust  type  and  well  preserved.  The  only  physical 
finding  of  importance  was  on  rectal  examination,  which  revealed 
a large,  hard,  globular  mass  of  faeces,  with  a slippery  surface,  acting 
as  a Tcctal  baU-valve.  This  mass  was  later  broken  up  digitally  and 
removed  with  complete  relief  of  all  symptoms. 

The  return  of  an  enema  unaltered  does  not  prove  that  the 
rectum  is  empty. 

Anaemia 

A young  man  complained  of  general  symptoms  of  anaemia 
which  had  developed  rather  rapidly.  He  had  not  noticed 
anything  peculiar  about  his  stools,  but  his  appearance  and 
history  suggested  that  the  anaemia  might  be  due  to  bleeding. 
Rectal  examination  produced  some  tarry  matter  on  the 
finger-stall,  and  the  diagnosis  of  bleeding  duodenal  ulcer 
was  established. 


Obscure  Pyrexia 

Here  is  a case  in  which  I failed  to  make  a rectal  examina- 
tion and  so  to  make  a correct  diagnosis. 

A young  man  was  taken  ill  with  slight  sore  throat,  fever,  and 
malaise.  At  the  time  of  my  visit  he  had  bad  an  evening  temperature 
of  101°  to  102°  for  two  nights,  and  it  had  now  risen  to  103°.  He  felt 
HI,  but  complained  of  nothing  localising.  There  had  been  no  shiver- 
ing, but  he  had  sweated  profusely.  Although  his  throat  was  redder 
than  normal  there  was  no  tonsillitis,  and  nothing  to  be  seen  to  explain 
his  temperature.  A routine  examination  of  his  systems  was  negative ; 
the  urine  was  chemically  normal;  the  leucocyte  count  was  7,800  cells 
per  cm  Although  I did  not  think  that  he  had  a septicaemia, 
I took  some  blood  for  cultivation.  Now  here  is  a point  in  the  history 
by  which  I had  not  been  sufficiently  impressed.  Two  months  pre- 

O 


101  ON  EXAMINING  THE  RECTUM 

viously  lie  had  gonorrhoea  for  the  second  time,  hut,  excepting  for 
a slight  morning  gleet,  he  Iwd  lost  all  his  symptoms.  There  was  no 
orchitis.  After  3 more  days  of  fever  he  developed  a profuse  purulent 
discharge  from  the  urethra,  and  the  temperature  fell.  A rectal 
examination  would  almost  certainly  have  revealed  a prostatic  abs- 
cess, and  would  have  saved  me  the  trouble  of  a blood-count  and  the 
patient  the  expense  of  a blood-culture. 

Conclusion 

There  are  certain  examinations  over  and  above  the 
routine  overhaul  of  the  systems  which  at  times  become 
a positive  duty.  They  are  examinations  open  to  all  and 
require  no  specialist  skill.  Among  them  are  (1)  naked-eye 
examination  of  the  stools ; (2)  microscopic  examination  of 
the  urinary’  sediments ; (8)  examination  of  the  fundus  oculi ; 
(4)  observations  on  the  blood -pressure ; (5)  estimations  of 
the  haemoglobin  and  inspection  of  blood-films ; (6)  exami- 
nation of  the  pelvic  organs  in  women ; and  (7),  and  last,  but 
by  no  means  least,  the  humble  examination  which  is  the 
subject  of  this  lecture. 


XIV 

BALL- VALVE  ACCUMULATIONS  IN  THE  RECTUM1 

The  impaction  of  hard  and  bulky  faeces  in  the  rectum, 
particularly  in  the  case  of  aged  and  infirm  persons,  has  long 
been  reckoned  among  the  causes  of  severe  constipation. 
Digital  or  instrumental  fragmentation  and  removal  of  the 
faecal  mass  is  the  accepted  treatment  when  enemata  are 
unavailing.  Occasionally  the  mass  becomes  moulded  into 
the  shape  of  a ball  or  ovoid,  which  distends  the  rectum  and, 
while  sufficiently  mobile  to  allow  the  escape  of  flatus  or 
fluid  material,  itself  resists  all  natural  efforts  at  expulsion. 

Hurst  [1]  devotes  a chapter  of  his  book  on  Constipation 
to  this  type  of  disorder,  and  on  p.  258  describes  the  case 
of  a child  aged  four  who  came  under  his  observation  with 
an  unusually  large  colonic  accumulation  above  a movable 
globular  mass  weighing  a quarter  of  a pound.  He  refers  to 
a description  of  similar  accumulations  in  old  subjects  by 
Curling  [2]  (1876),  and  accords  to  Simpson  [3]  (1849),  who 
specifically  employs  the  term  ‘ball-valve’,  the  priority  for 
having  furnished  the  first  account  of  the  condition.  A still 
earlier  account  is  to  be  found  in  the  writings  of  William 
Heberden  [4],  who,  in  a single  brief  paragraph,  aptly  depicts 
the  main  symptoms  and  complications  as  follows:  ‘The 
faeces  sometimes  lie  in  the  rectum  for  many  months,  and  are 
collected  into  a large  hard  mass,  which  cannot  be  voided 
without  the  help  of  a surgeon.  The  signs  of  this  are,  pains 
in  the  belly ; a constant  desire  to  go  to  stool,  even  just  after 
an  evacuation;  none  but  liquid  faeces  are  ever  voided;  and 
the  disorder  is  attended  with  a difficulty  of  making  water.  ’ 

Many  examples  of  this  condition  have  come  to  my  notice 
in  recent  years.  These  might  appear  altogether  too  trivial, 
and  the  nature  of  the  symptoms  too  obvious,  to  be  worth 
recording,  but  I am  persuaded  to  do  so  for  the  following 
reasons: 

(1)  In  6 of  7 cases  seen  at  one  period  the  cause  of  the 
1 Guy' a JIosp.  Reports,  lt>20,  tori.  175. 


100  BALL-VALVE  ACCUMULATIONS  IN  THE  RECTUM 
symptoms  had  passed  unrecognized  by  the  medical  men  and 
nurses  in  attendance.  Three  of  these  cases  (Cases  2,  5,  and 
7)  were  under  close  observation  in  hospital.  The  seventh 
patient  was  a medical  man  who  was  able  to  appreciate  the 
cause  of  his  discomforts. 

(2)  The  direct  or  complicating  symptoms  in  5 of  the  cases 
were  so  severe  and  distressing  as  to  call  urgently  for  relief, 
and  in  3 cases  (Cases  3,  4,  and  G)  had  prompted  a suspicion 
of  some  more  serious  malady. 

(3)  In  3 cases  (Cases  1,  2,  and  7)  the  trouble  was  a direct 
result  of  an  X-ray  examination  with  barium  meal  or  enema, 
and  the  accumulation  was  largely  composed  of  barium 
sulphate. 

In  the  histories  of  the  first  3 cases  there  is  nothing  parti- 
cularly noteworthy. 

Case  1.  A medical  man,  aged  64, 2md  an  obstructive  carcinoma  of 
the  splenic  flexure.  He  had  been  examined  with  a barium  enema  in 
order  to  locate  the  point  of  the  obstruction.  During  the  ensuing  *S 
hours  he  expressed  himself  as  unable  to  void  the  ‘cemcnt-like’  ac- 
cumulation by  natural  efforts,  and  was  compelled  to  relieve  himself 
digitally. 

Case  2.  A lady,  aged  CO,  had  undergone  a routine  examination  of 
the  alimentary  tract  after  a barium  meal.  A day  or  two  later  she  was 
in  great  discomfort,  and  this  the  nurse  had  been  unable  to  relieve 
with  enemata.  Rectal  examination  revealed  a globular,  putty-like 
mass  in  the  rectum,  which  could  be  moved  about  by  the  examining 
finger  and  which  had  to  be  broken  up  before  relief  could  be  obtained. 

Case  0.  An  old  man  was  sent  to  my  Out-Patients  for  chronic 
diarrhoea,  and  was  suspected  of  having  a malignant  growth  of  the 
bowel.  Rectal  examination  revealed  a similar  collection  of  putty-like 
faeces,  obviously  acting  as  a baH- valve. 

In  each  of  the  four  remaining  cases  there  were  special 
features  which  warrant  a fuller  description. 

Case  4.  A marine  engineer,  aged  39,  had  been  out  of  employment 
for  two  years  and  often  rather  short  of  food.  He  eventually  obtained 
work  on  a tramp  steamer  on  which  the  sanitary  conditions  were  poor, 
and  while  on  a voyage  to  Gibraltar  experienced  pain  in  the  lower 
abdomen  which  developed  an  hour  after  food.  This  became  worse 
and  worse  each  day,  and  at  Gibraltar  he  was  put  ashore  and  sent  to 
hospital  with  a diagnosis  of  gastric  ulcer.  He  lost  his  pain  after  three 
days  on  a milk  diet  and  was  later  invalided  home.  tYhen  I saw  him 
be  stated  that  ever  since  admission  to  the  hospital  he  had  been 


BALL-VALVE  ACCUMULATIONS  IN  THE  RECTUM  197 
troubled  with  constipation,  defaecation  had  been  very  difficult,  and 
he  had  always  felt  as  if  the  bowel  contained  something  more  to  be 
voided.  His  weight,  which  had  been  10  st.  7 lb.  for  years,  had  fallen 
to  8 st.  The  abdomen  was  everywhere  slightly  distended  and  tym- 
panitic, but  nowhere  tender,  and  nothing  unusual  was  felt  excepting 
for  a resistance  rather  like  a full  bladder  above  the  pubes.  Rectal 
examination  revealed  an  enormous  faecal  accumulation  noting  a3  a 
ball-valve  and  obviously  accounting  for  his  rectal  discomforts.  The 
examination  caused  great  pain.  A small  amount  of  the  accumulation 
was  removed  digitally,  and  immediately  afterwards  he  had  the  most 
successful  action  of  his  bowels  that  he  had  had  for  weeks.  During  the 
next  few  days  the  bowel  was  cleared  with  the  help  of  enemata  and  all 
hi3  symptoms  disappeared.  He  was  then  admitted  to  hospital  for 
a routine  examination  of  his  alimentary  tract.  No  signs  of  disease 
were  found.  He  remained  well,  and  rapidly  gained  weight. 

Case  5.  An  elderly  and  obese  woman  was  admitted  to  Guy’s 
Hospital  under  roy  care  on  account  of  glycosuria.  Shortly  after  ad- 
mission she  began  to  complain  of  pain  in  the  lower  abdomen  and 
rectum  and  developed  complete  retention  of  urine.  On  account  of 
this  latter  symptom  I was  asked  by  my  House  Physician  to  see  her. 
Catheterization  had  then  been  necessary  for  24  hours.  I suspected 
a Tecta!  accumulation,  and  examination  revealed  a glohular  mass 
acting  as  a ball- valve.  The  examination  was  very  painful.  The 
mass  was  broken  up  under  an  anaesthetic  and  the  pain  and  retention 
were  relieved. 

Case  0.  I was  called  to  see  a case  in  consultation  with  the  following 
history:  The  patient  was  a woman,  aged  CO.  She  had  been  under 
observation  during  the  past  2 years  for  dyspeptic  symptoms  with 
epigastric  and  subscapular  pains.  Two  weeks  previously  she  had 
vomited  a little  blood.  A week  later  she  had  a more  definite  haema* 
temesis,  became  collapsed,  and  afterwards  passed  large  tarry  motions. 
As  the  colon  seemed  to  be  overloaded,  she  was  ordered  enemata, 
which  at  first  brought  away  some  rather  solid  material  but  later  were 
returned  clear.  For  the  last  4 or  G days  she  had  been  complaining  of 
constant  pain  in  the  rectum,  pain  in  the  lower  abdomen,  ‘bearing 
down’  sensations,  and  much  anxiety  and  misery.  Her  doctor  was 
afraid  that  she  might  have  some  malignant  disease  of  the  bowel.  The 
patient,  who  was  a multipara,  stated  that  ‘the  pains  were  like  bad 
labour  pains'.  She  also  had  pain  on  passing  water.  There  was 
moderate  tenderness  over  the  lower  abdomen,  more  particularly  on 
the  left  side,  where  there  was  a sense  of  deep  resistance  suggesting  a 
greatly  distended  pelvic  colon.  Itectal  examination  showed  an  enor- 
mous ball-valve  accumulation  of  faecal  material,  hard,  with  a greasy 
surface,  receding  before  the  examining  finger,  and  feeling  in  shape  and 
size  not  unlike  a foetal  head.  The  examination  caused  intense  pain. 
On  the  next  day  she  was  given  an  anaesthetic,  the  accumulation 


103  BALL-VALVE  ACCUMULATIONS  IN  THE  RECTUM 
was  broken  up  and  removed  by  lavage  with  prompt  relief  of  all  her 
symptoms. 

Matthews  Duncan  [5]  reported  a very  similar  case  in  which 
the  patient  had  been  thought  to  be  dying  of  a rectal  car- 
cinoma. 

Case  7.  A man,  aged  C3,  was  sent  to  me  on  account  of  a large  hard 
tumour  in  the  epigastrium.  There  was  also  a gland  above  the  left 
clavicle  and  a swelling  of  the  right  testicle.  It  was  eventually  decided 
that  the  mass  in  the  epigastrium  consisted  of  retroperitoneal  deposits 
from  a malignant  growth  of  the  testicle,  but  in  the  early  stages  steps 
were  taken  to  exclude  a primary  alimentary  carcinoma.  For  48  hours 
or  more  after  the  X-ray  examination  tliis  patient  was  in  the  greatest 
distress,  had  frequent  and  urgent  calls  to  stool,  and  much  ‘bearing 
down*  pain.  Within  the  space  of  twenty-four  hours  he  visited  the 
lavatory  on  thirty  occasions,  but  was  never  able  to  pass  more  than  a 
very  small  amount  of  semi-fluid  material.  He  was  in  hospital  and  had 
been  treated  with  purgatives  and  enemata  without  result.  Neither 
the  resident  medical  ofllcer  nor  the  sister  was  familiar  with  the  symp- 
toms. Rectal  examination  showed  a large  globular  mass  in  the  rectum 
with  a greasy  surface;  it  was  extremely  hard,  and  consisted  mostly 
of  barium.  The  examination  caused  exquisite  pain.  The  mass  was 
finally  broken  up  under  an  anaesthetic  and  cleared  away  with 
enemata. 

It  should  be  noted  that  with  one  exception  these  patients 
were  aged  60  years  or  upwards.  Doubtless  their  age  or 
infirmity  had  combined  to  diminish  the  expulsive  power  of 
the  rectal  muscles.  The  clinical  symptoms  cannot  be  more 
concisely  described  than  in  the  words  of  Ilcberden  quoted 
above,  but  it  is  necessary  to  have  witnessed  the  sufferings 
of  these  patients  to  appreciate  how  severe  they  may  be. 
Case  6 likened  her  sensations  to  ‘bad  labour  pains’,  and 
their  rhythmical  recurrence  during  the  examination  was 
very  reminiscent  of  the  pangs  of  childbirth.  In  Simpson’s 
cases  [8]  also  the  pains  were  likened  to  those  of  labour. 
Case  7,  a very  plucky  man  who  bore  his  illness  bravely, 
suffered  great  misery  and  made  as  many  as  thirty  attempts 
to  empty  the  bowel  in  the  course  of  one  day.  The  pain  is 
felt  both  in  the  rectum  and  in  the  lower  abdomen.  Presum- 
ably as  the  result  of  reflex  anal  spasm  the  rectal  examina- 
tion in  every  case  caused  great  pain,  resembling  that  induced 
by  digital  examination  in  cases  of  anal  fissure.  The  factors 


BALL-VALVE  ACCUMULATIONS  IN  THE  RECTUM  199 
which  prevent  the  evacuation  of  these  faecai  masses  would 
seem  to  include  their  solid  consistency,  spherical  shape,  and 
smooth  greasy  surface.  In  three  instances  (Cases  2, 6,  and  7) 
the  doctor  or  nurse  in  attendance  had  been  deceived  into 
thinking  that  there  could  be  no  rectal  accumulation  be- 
cause enemata  had  been  returned  clear. 

Summary 

The  causes,  symptoms,  diagnosis,  and  treatment  of  ball- 
valve  accumulations  of  faeces  in  the  rectum  may  be  sum- 
marized as  follows: 

(1)  Causes,  (a)  A recent  gastric  or  duodenal  haemorrhage, 
a barium  meal  or  enema,  or  a milk  diet.  These  may  impart 
such  a consistency  and  superficial  greasiness  to  the  faecal 
mass  as  to  render  it  difficult  of  passage.  (6)  Dehydration  as 
the  result  of  recent  haemorrhage,  or  of  fasting  or  diabetes. 
Any  of  these  may  help  to  make  the  stools  unnaturally  solid, 
while  the  long  sojourn  of  the  mass  in  the  rectum  results  in 
further  desiccation.  Hobson  [6]  described  6 cases  of  ‘acute 
faecal  impaction  in  the  rectum’  consequent  upon  diarrhoea 
or  haemorrhage,  (c)  Old  age  or  infirmity.  These,  combined 
with  the  fatigue  of  repeated  calls  to  stool  and  reflex  anal 
spasm,  diminish  the  expulsive  power  of  the  muscles  of  de- 
faecation. 

(2)  The  Symptoms  include:  (a)  Frequent  and  urgent  calls 
to  stool  with  no  result  or  small  fluid  results.  ( b ) A feeling 
after  evacuation  as  though  there  were  still  something 
further  to  expel,  (c)  Severe  recurring  pain  of  a peristaltic 
kind  {rectal  colic)  and  lower  abdominal  colic.  ( d ) Painful 
anal  spasms  which  are  intensified  by  digital  examination, 
(e)  Difficulty  of  micturition  or  actual  retention  of  urine. 
(/)  Failure  to  secure  relief  by  purgatives  or  enemata  unless 
the  mass  be  first  broken  up. 

(3)  The  Diagnosis  is  at  once  made  by  a digital  examina- 
tion. This  reveals  a large  solid,  putty-like  globular  mass, 
which  often  recedes  from  the  examining  finger  and,  owing 
to  its  slippery  surface,  may  be  difficult  to  grasp. 

(4)  Treatment  consists  in  the  fragmentation  and  piece- 
meal removal  of  the  mass,  and  clearance  of  the  rectum  by 


200  BALL-VALVE  ACCUMULATION'S  IN  THE  RECTUM 
repeated  lavage.  For  this  operation  the  administration  of 
an  anaesthetic  is  usually  necessary.  The  handle  of  a spoon 
is  a useful  instrument,  although  much  of  the  operation 
must  be  performed  with  the  fingers.  As  a preventive  measure 
it  should  come  within  the  province  of  the  radiologist  to 
advise  proper  supervision  of  the  evacuations  in  old  or  feeble 
persons  who  have  been  subjected  to  examinations  of  the 
alimentary  tract  after  a barium  meal  or  enema. 

REFERENCES 

1.  Hurst,  A.  F. : Constipation  and  Allied  Intestinal  Disorders,  pp.  ICO 

and  258.  2nd  edition,  London,  1019. 

2.  Curling,  T.  B.j  Diseases  of  the  Itectum,  p.  187.  4th  edition,  Lon- 

don, 1870. 

3.  Simpson,  J.  V.s  Edinburgh  Monthly  Journal  of  Medical  Science, 

1819,  ix.  705. 

4.  llnnr.nnEs,  \Y. : Commentaries  on  IJ/e  History  and  Cure  of  Diseases, 

p.  14.  4th  edition,  London,  181C. 

5.  Matthews  Duncan,  J.:  Medical  Times  and  Gazette,  1879,  ii.  522. 
0,  Robson,  W.  M.:  Drit.  Med.  Joum .,  1003,  i.  10-11. 


XV 

VISCERAL  NEUROSES1 
Introductory 


In  the  preface  to  his  book  on  Diseases  of  the  Nervous  System, 
written  over  sixty  years  ago.  Sir  Samuel  Wilks  remarks:  ‘It 
is  undoubtedly  true  that  there  is  not  a single  organic  disease 
of  the  nervous  system  which  may  not  be  simulated  by  a 
functional  and  curable  one.’  The  same  might  be  said  of 
diseases  affecting  the  hollow  viscera  which,  depending  for 
their  natural  behaviour  upon  a proper  co-ordination  of 
vagal  and  sympathetic  impulses,  readily  complain  when 
this  delicate  harmony  is  disturbed  or  destroyed.  That  the 
symptoms  of  organic  visceral  disease  should  be  simulated 
by  those  of  functional  disorder  is  no  matter  for  surprise 
when  we  pause  to  consider  that  all  subjective  symptoms 
express  only  perturbations  of  function  and  that  such  per- 
turbations may  depend  upon  a great  variety  of  activating 
or  inhibitory  stimuli  applied  at  various  points  in  the  reflex 
arc.  Angina  pectoris,  now  held  to  proclaim  an  ischaemia 
of  the  myocardium,  is  due  in  most  instances  to  coronary 
arteriosclerosis,  but  it  may  also  be  caused  by  coronary 
spasm  resulting  from  anxiety  or  tobacco,  or  occur  as  a local 
symptom  of  anaemia. 

Visceral  neuroses  may  be  held  to  include  those  disorders 
of  visceral  motility  and  sensibility  which  occur  in  the 
absence  of  organic  disease.  They  are  of  common  occurrence 
in  daily  practice,  and  many  of  them  are  trivial  in  their 
physical  effects,  but  it  must  also  be  conceded  that  they  are 
capable  of  causingmuch  bodily  distress  and  anxiety  of  mind 
in  their  victims.  Their  recognition  in  most  cases  is  com- 
paratively easy,  but  in  others  their  differentiation  from 
disorders  due  to  structural  disease  can  be  extremely  diffi- 
cult. To  regard  them  as  expressive  of  organic  disease  is 
sometimes  to  do  a grave  injustice  to  patients  and  may  even 

1 Based  on  an  address  given  to  the  Bristol  Branch  of  the  British  Medical 
Association,  80  May  1934  (Gut/’*  Hosp.  Reports,  1034,  lxxxiv.  430). 


202  VISCERAL  NEUROSES 

be  ns  hurtful  in  the  long  run  os  to  label  an  organic  condition 
‘functional’.  Unnecessary  invalidism  is  established  and 
unnecessary  operations  arc  performed  every  day  because  of 
these  difficulties  and  failures  of  differentiation. 

I believe  that  our  forebears,  before  the  days  of  radiological, 
biochemical,  and  cardiographic  diagnosis,  were  often  more 
efficient  in  these  differentiations  than  -we  are  to-day,  for 
although  these  and  other  technical  refinements  have  enabled 
us  to  understand  and  to  recognize,  or  to  recognize  earlier 
and  more  surely,  a host  of  structural  changes  of  which  we 
could  not  previously  be  sure  by  the  exercise  of  our  clinical 
wits  alone,  they  have  also  had  the  effect  of  concentrating 
our  thoughts  on  objective  methods  and  of  creating  false 
mechanical  and  chemical  concepts,  and,  what  is  worse,  of 
encouraging  a certain  slackness  in  clinical  history-taking 
and  symptom-analysis.  But  the  pendulum  will  swing  again, 
and  with  adjustments  of  thought  and  a wiser  curriculum  it 
should  be  possible  for  the  next  generation  or  the  generation 
after  that  to  surpass  our  own  and  all  others  in  bed-side 
wisdom. 

It  is  the  purpose  of  this  paper  to  make  a small  contribu- 
tion to  the  study  of  the  visceral  neuroses,  by  considering 
the  natural  history  and  symptomatology,  the  differential 
diagnosis,  and  treatment  of  certain  neuroses  affecting  the 
gullet,  the  stomach,  the  colon,  the  rectum,  the  bladder,  and 
the  heart. 

The  Nature  of  the  Visceral  Neuroses 

Of  the  nature  of  all  of  these  neuroses  it  may  be  said  that 
they  are  due  to  a loss  of  ncuro-muscular  rhythm.  Sir  James 
Paget  [I]  in  a classical  paper,  ‘On  Stammering  with  other 
organs  than  those  of  Speech’,  in  which  he  discusses  the 
stammering  bladder  in  particular,  wrote  as  follows:  ‘Stam- 
mering, in  whatever  organs,  appears  due  to  a want  of  con- 
cord between  certain  muscles  that  must  contract  for  the 
expulsion  of  something,  and  others  that  must  at  the  same 
time  relax  to  permit  the  thing  to  be  expelled.  ’ The  result,  as 
with  the  speech-stammerer,  is  inhibition  or  disorderly  action 
with  distress  or,  in  the  case  of  some  viscera,  actual  pain. 


VISCERAL  NEUROSES  203 

The  victims  of  visceral  stammering  are  commonly  of  kin- 
dred temperament  with  the  speech-stammerers.  Again  and 
again  we  can  trace  the  symptoms  of  which  they  complain  to 
a failure  of  relaxation  of  plain  muscle,  to  a positive  spasm, 
or  to  a loss  of  the  normal  tonic  and  peristaltic  habit,  dis- 
turbances which  it  has  been  customary  to  attribute 
(employing,  I believe,  too  dubious  a term  and  too  narrow  a 
conception)  to  the  influence  of  ‘vagotonia’. 

The  Mode  of  Initiation  of  Visceral  Neuroses 

(1)  The  origins  of  a visceral  neurosis  may  be  found  in  a 
previous  but  finally  departed  organic  injury  in  the  shape 
of  an  inflammation  or  irritation.  Thus  a dysentery  may 
leave  in  its  wake  a spastic  or  irritable  colon.  A completely 
cured  cystitis  may  be  followed  by  a nervous  frequency. 
These  consequences  are  closely  comparable  with  the  blepha- 
rospasm which  succeeds  a conjunctival  irritation,  or  the 
asthma  which  may  be  initiated  by  bronchitis. 

(2)  A visceral  neurosis  may  occur  in  consequence  of  a 
specific  sensitization  or  allergy.  Certain  dyspepsias  and  spas- 
modic disorders  of  the  colon  can  be  traced  to  food-idiosyn- 
crasies or  tobacco,  and,  although  I believe  it  to  be  very  rare, 
tobacco-angina  may  also  be  mentioned  in  the  same  category. 
As  with  asthma,  however,  it  is  unusual  for  the  symptoms 
to  be  traceable  always  and  only  to  a single  specific  factor. 

(8)  External  agencies  such  as  cold  and  the  general 
physical  effects  of  fatigue,  emotion,  and  worry  are  common 
precipitating  factors  or  'triggers’  for  the  visceral  neuroses. 

(4)  The  general  state  of  physical  tension  accompanying 
chronic  anxiety  prepares  the  ground  for  many  of  the  visceral 
neuroses. 

(5)  Commonly  enough  some  combination  of  the  above- 
mentioned  influences  can  be  clearly  revealed  in  individual 
case  histories 

(6)  In  addition  to  and  underlying  all  these  factors,  we 
discover  good  grounds  for  including  diathesis  or  the  in- 
herited (or  constitutional)  factor.  We  know  that  these 
visceral  disturbances  afllict  persons  of  a certain  type  and 
temperament,  generally  recognized  as  alert,  restless,  or 


201  VISCERAL  NEUT10SES 

‘highly  strung’,  and  that  their  occurrence  among  plilcgma* 
tic  types  is  conspicuously  rare.  We  find  that  multiple  vis- 
ceral neuroses  occur  simultaneously  or  at  different  times  in 
the  same  individual ; that  the  same  visceral  neurosis  occurs 
in  more  than  one  member  of  the  same  family;  or  that 
there  is  a liability  to  a variety  of  visceral  and  other 
neuroses  discoverable  in  various  members  of  a family.  Thus 
asthma,  hay-fever,  migraine,  and  spastic  colon  will  crop 
up  among  the  near  relations  of  a sufferer  from  any  one 
of  these  disorders,  and  I shall  have  other  associations  to 
describe. 

TnE  Mode  of  Perpetuation  of  a Visceral  Neurosis 

Given  a super-sensitive  nervous  mechanism,  it  is  clear 
that  smaller  adverse  stimuli  will  be  necessary  to  create  or 
maintain  a visceral  disturbance  than  in  the  case  of  a more 
balanced  mechanism.  In  such  case  a slight  degree  of  con- 
stipation, a small  dose  of  purgative,  or  an  indigestible 
residue  in  the  diet  may  evoke  a tonic  over-action  in  the 
colon.  Again,  when  cold  or  fatigue  or  worry  are  also  opera- 
tive, the  local  stimuli  requisite  for  the  over-action  may  be 
smaller  still.  This  buttressing  or  reinforcement  of  one 
adverse  factor  by  another  is,  in  all  probability,  a common 
cause  of  perpetuation  of  symptoms. 

The  anxiety  of  mind  and  the  physical  fatigue  and  irri- 
tability created  by  the  physical  symptoms  themselves, 
uncertainty  ns  to  their  meaning  and  apprehension  of  their 
recurrence,  also  play  their  part.  Like  the  conditioned  re- 
flexes in  Pavlov’s  dogs,  and  given  an  effective  initial 
stimulus,  the  susceptibility  of  the  patient  is  constantly 
increased  by  repetition.  Conversely,  in  treatment,  anything 
which  serves  to  lengthen  the  interval  between  ‘attacks’  or 
to  eliminate  one  or  more  of  the  conditioning  stimuli  is  cal- 
culated to  reduce  susceptibility. 

I believe  that  our  greatest  difficulty  in  the  management 
of  cases  of  asthma,  paroxysmal  tachycardia,  spastic  colon, 
migraine,  and  all  the  other  paroxysmal  neuroses  lies,  not 
so  much  in  our  inability  to  discover  effective  ‘triggers’  as 
in  our  inability  to  cope  with  this  constantly  enhanced 


205 


VISCERAL  NEUROSES 
susceptibility  or  repeated  conditioning  of  the  exaggerated 
reflex  by  increasingly  infinitesimal  and  varied  stimuli. 

Oesophageal  Neuroses 

Among  the  commoner  and  less  serious  oesophageal 
neuroses  we  may  include  ‘globus’  and  ‘heartburn’,  but  as 
these  symptoms  rarely  suggest  organic  disease  I shall  not 
deal  with  them  at  length.  Both  of  them  will  have  been  an 
occasional  experience  for  most  of  us — ‘globus’  in  times  of 
grief  as  the  ‘lump  in  the  throat’,  and  ‘heartburn’,  some- 
times through  rush  or  indiscretion  but  often  enough  for  no 
discoverable  cause,  as  an  unpleasant  burning  sensation  felt 
at  various  levels  behind  the  sternum. 

Sometimes,  however,  these  symptoms  become  so  fre- 
quent or  persistent  as  to  cause  much  misery,  and  objective 
investigations  into  cause  may  be  completely  unavailing. 
The  occurrence  of  heartburn  in  the  later  months  of  preg- 
nancy suggests  that  physical  or  biochemical  factors  can 
promote  it,  but  in  what  way  we  do  not  know.  Odd  circum- 
stances null  sometimes  cause  it.  Thus,  one  man  told  me 
that  he  invariably  had  heartburn  after  coitus.  Globus  is 
probably  due  to  a local  tonic  ring-contraction  of  slight 
degree ; heartburn  to  increased  tonic  and  peristaltic  action 
[2],  perhaps  with  ‘squeezing’  of  the  oesophageal  mucosa. 
As  examples  of  troublesome  globus  let  me  quote  two  cases. 

Case  1.  The  first  was  that  of  a nervous  Jewish  boy  aged  14,  clever 
and  doing  well  at  school.  Up  to  the  age  of  12  he  had  suffered  from 
enuresis.  His  complaint  was  that  for  15  months  he  had  experienced 
a feeling  of  a lump  under  his  sternum,  first  of  all  during  swallowing 
and  latterly  nearly  all  the  time.  He  also  had  heartburn.  He  had 
seen  many  doctors  and  had  been  X-rayed  with  negative  result.  He 
suffered  no  difficulty  in  swallowing  or  regurgitation  and  was  otherwise 
very  well.  Excitement  and  examinations  aggravated  the  symptom. 

Case  2.  A married  woman,  aged  45,  had  been  troubled  for  a year 
by  a ‘lump  in  the  throat’,  and  had  consulted  orthodox  and  unortho- 
dox medical  opinion  and  a throat  specialist,  obtaining  no  relief.  The 
symptom  first  developed  at  a time  of  great  anxiety  when  she  dis- 
covered a small  breast-tumour.  She  looked  very  healthy  and  had  just 
completed  a walking-tour  in  Germany,  walking  from  10  to  20  miles  a 
day,  and  expressed  herself  as  ‘bursting  with  energy’.  The  symptom, 


200 


VISCERAL  NEUROSES 
initiated  by  a mental  stress,  h3d  received  treatment  with  medicines 
instead  of  reassurance  and  explanation. 

The  neuroses  of  the  gullet  which  simulate  organic  disease 
are  much  more  rare.  In  these  spasm  giving  rise  to  pain, 
difficulty  in  swallowing,  and  regurgitation  of  food  may 
occur.  They  have  to  be  distinguished  from  benign  and 
malignant  stricture,  achalasia  of  the  cardia,  reflex  spasm 
from  benign  or  malignant  ulceration  at  the  cardiac  end  of 
the  stomach,  and  the  dysphagia  with  anaemia  and  glossitis 
sometimes  referred  to  as  ‘ Plummer- Vincent’s  syndrome’. 
Radiology  and  oesophagoscopy  have  greatly  facilitated  these 
differentiations,  but  there  are  usually  distinctive  features 
in  the  clinical  history  too.  The  neuroses  are  characterized  by 
their  intermittcncy  and  association  with  nervous  causes  and 
with  the  neurotic  temperament.  The  continued  and  progres- 
sive pain  and  difficulty,  more  at  first  with  solids  than  with 
fluids,  encountered  in  malignant  stricture,  and  the  accurate 
descriptions  of  food  retention  and  bulky  regurgitation  of 
achalasia  are  not  features  of  the  neuroses,  as  will  be  seen 
from  the  following  cases. 

Case  3.  A well-built  nervous  man  aged  49,  with  a family  history 
of  gout  in  his  father  and  asthma  in  his  son,  and  a personal  history  of 
gout,  migraine,  and  iritis,  complained  that  for  10  years  he  had  been 
liable  nt  long  intervals  to  attacks  of  severe  pain  at  the  lower  end  of  the 
sternum,  radiating  up  into  the  chest  and  the  jaws.  lie  declared  that 
it  would  be  unendurable  if  it  lasted  more  than  a few  seconds.  This 
description  at  once  suggested  angina  pectoris,  but  further  inquiry 
showed  that  it  had  never  been  induced  by  walking  or  effort,  that  it 
generally  came  on  while  he  was  stooping  over  his  desk,  that  it  could 
be  immediately  relieved  if  he  was  able  to  swallow  some  fluid  or  solid, 
and  that  on  swallowing  he  heard  a distinct  dick  as  the  pain  departed. 
With  reassurance  and  general  treatment  the  symptoms  have  remained 
in  abeyance  for  many  months.  The  patient  later  consulted  me  for 
extra-systoles. 

Case  4.1  A woman,  aged  69,  was  troubled  for  a period  of  3 years 

1 A recent  re-examination  of  this  case  has  revealed  an  organic  cause  for 
the  symptoms.  In  certain  postures  only  a very  small  hernia  of  the  stomach 
through  the  oesophageal  opening  can  be  revealed  radiologically.  It  is 
worthy  of  note  that  this  patient  showed  none  of  the  associated  neuroses 
which  are  a feature  of  the  majority  of  the  cases  described  in  this  paper. 
Case  3,  I now  have  no  doubt,  was  also  a case  of  hiatus  hernia.  Globus, 
heartburn,  and  painless  anxiety  dysphagia  thus  remain  the  only  common 
neuroses  of  the  gullet. 


207 


VISCERAL  NEUROSES 
by  a frequent  burning  sensation  in  the  course  of  the  gullet  to  which 
were  added  curious  spasms  while  eating  in  which  the  food  would  not 
go  down.  At  times  she  was  compelled  to  leave  the  table  and  bring 
up  a mouthful  of  food.  These  episodes  were  sometimes  followed  by 
hiccups.  Radiograms  showed  a norma!  gullet.  A fuller  dietary  than 
had  been  allowed,  alkalis,  and  luminal  brought  about  a marked 
amelioration  of  symptoms. 

Cask  5.  A nervous  Welsh  woman,  giving  a family  history  of  in- 
somnia, from  irliich  she  herself  suffered,  and  of  ‘nervous  breakdown’ 
in  a sister  and  shell-shock  in  a brother,  complained  of  a sensation  of 
‘lump  in  the  throat’.  This  would  he  worse  at  night  and  on  sitting  up 
she  maintained  that  she  could  hear  ‘food  trickling  through  it’.  On 
three  occasions  she  had  brought  up  food.  She  had  always  experienced 
difficulty  la  holding  her  water.  X-ray  examination  with  emulsions 
of  varying  consistency  failed  to  reveal  any  abnormality  of  the  gullet. 

Cask  fi.  A nervous  woman,  aged  43,  after  a tiring  day  was  seized 
with  an  inability  to  swallow  while  eating  fish.  This  inability  persisted 
for  10  hours,  during  which  she  could  not  even  swallow  fluids  or  her 
own  saliva.  There  was  no  pain.  During  the  previous  4 years  she  had 
experienced  the  same  symptom  on  several  occasions,  but  it  had  only 
lasted  for  about  10  minutes.  Eating  fish  when  tired  had  been  the 
chief  precipitating  factor.  There  uas  no  radiological  evidence  of  any 
disease  of  the  oesophagus. 

Gastric  Neuroses 

These  are  so  numerous  and  varied  that  they  would  require 
a chapter  to  themselves.  They  may  be  expressed  by  pain, 
discomfort,  nausea  or  vomiting,  flatulence,  or  anorexia  in 
varying  combinations.  Air-swallowing  is  a frequent  accom- 
paniment. Those  which  simulate  organic  disease  such  as 
gastric  or  duodenal  ulcer  are  the  most  important  in  that 
inappropriate  treatments  may  be  deemed  necessary  and 
invalidism  increased  by  the  idea  of  graver  trouble.  Although 
operations  are  now  less  frequently  performed  for  the  gastric 
than  for  the  colonic  neuroses  there  has  been  too  long  a tale 
of  them  in  past  years. 

In  the  comparatively  few  cases  of  genuine  allergic 
dyspepsia  which  I have  encountered,  the  symptoms  have 
sometimes  been  severe  enough  to  suggest  organic  disease,  but 
histories  of  food-poisoning  or  food-idiosyncrasy,  an  associa- 
tion with  urticaria  or  angio-neurotic  oedema,  and  negative 
radiological  studies  have  served  to  complete  the  diagnosis. 


203  VISCERAL  NEUROSES 

Case  7.  A woman  of  sensitive  type  nnd  with  too  little  to  occupy 
her,  complained  of  gastric  symptoms  developing,  as  in  duodenal  ulcer, 
from  2 to  3 hours  after  food  and,  also  like  duodena]  ulcer,  recurring 
at  intervals  of  a few  montlis  nnd  lasting  for  2 or  3 weeks.  On  inquiry, 
however,  the  sensation  was  not  the  usual  gnawing  pain,  but  a ‘feeling 
of  lump  in  the  epigastrium’.  This  ‘feeling  of  lump’  already  mentioned 
as  distinctive  of  globus,  may  also  be  described  in  gastric,  colonic,  nnd 
rectal  neuroses.  In  her  case  it  probably  expressed  a pyloric  contrac- 
tion occurring  when  the  stomach  was  empty  or  emptying.  She  also 
mentioned  nocturnal  attacks  of  rectal  pain,  and  digital  examination 
showed  a rectal  ring-spasm. 

Case  8.  A chronic  asthmatic,  male,  aged  52,  complained  of  ‘feel- 
ings of  constriction’  in  the  stomach,  worse  when  he  was  empty  and 
eased  by  food.  Radiological  examination  with  the  barium  meat  on 
two  occasions  showed  only  a very  rapidly  emptying  organ  and  no 
evidence  of  gastric  or  duodenal  ulceration. 

Case  0.  Following  upon  a gastric  upset  attributed  to  flsb-poisoning, 
nnd  accompanied  by  a generalized  rash,  a young  woman  developed 
dyspeptic  attacks  cliaractcrizcd  by  epigastric  or  hypogastric  pain 
commonly  relieved  by  food.  There  was  marked  aggravation  by 
worry,  cold,  chocolate,  and  beef.  Dietetic  care,  rest,  and  belladonna 
brought  partial  relief. 

Case  10.  It  is  important  to  remember  that  the  victim  of  a visceral 
neurosis  may  also  develop  organic  disease.  As  a reminder  of  this  let 
me  quote  against  myself  a further  case  of  an  asthmatic  and  highly 
nervous  Jew  who  had  been  troubled  for  7 or  8 years  by  vomiting 
attacks.  Investigated  in  a well-known  clinic  in  1021,  no  organic 
disease  was  found.  In  November  1928  a Berlin  radiologist  diagnosed 
ulcer.  I saw  him  in  March  1920,  for  nausea  when  tired  or  empty,  and 
found  no  sign  of  organic  trouble,  and  again  on  5 November  1030, 
when  he  brought  films  from  another  clinic  in  Germany  purporting 
to  show  the  scar  of  o healed  duodenal  ulcer.  Vomiting  was  now  once 
more  a feature,  but,  persuaded  by  his  general  nervous  state,  I stUI 
regarded  the  case  as  one  of  gastric  neurosis  with  pyloric  spasm.  At 
the  end  of  that  month,  as  he  had  had  sickness  again  and  once  vomited 
raisins  at  2 a.m.f  which  he  had  taken  atlunch-time,  I had  him  X-rayed 
once  more.  An  intense  spasm  of  the  pjiorus,  with  some  delay,  was 
reported,  but  no  visible  lesion.  Nearly  a year  later  he  was  operated 
on  for  a carcinoma  of  the  pylorus  and  did  not  survive  the  resection. 
It  is  possible  that  lie  may  originally  have  had  a benign  ulcer,  but  be 
can  scarcely  have  had  a carcinoma  for  so  many  years. 

Colonic  Neuroses 

Of  the  neuroses  affecting  the  alimentary  tract  the  colonic 
neuroses,  after  the  gastric  neuroses,  are  the  roost  frequent. 


200 


VISCERAL  NEUROSES 
They  are  also  more  often  rais-diagnosed  than  the  others 
notwithstanding  that  they  present,  as  a rule,  a precise 
clinical  picture  and  quite  commonly  confirmatory  objective 
signs.  As  I have  discussed  them  fully  in  Lectures  XI  and 
XII I shall  not  dwell  upon  them  in  detail.  Suffice  it  to  say 
that  the  most  important  type,  sometimes  called  the  spastic 
colon,  is  characterized  by  a dull,  steady  ache  or  sometimes 
a much  more  severe  pain  in  the  ascending,  descending,  or 
transverse  colon  and  that  the  colon  can  often  be  palpated  in 
its  tonic  contracted  state.  It  leads  to  diagnoses  of  appen- 
dicitis (in  one-third  of  a personal  series  of  50  cases  the 
appendix  had  been  removed),  of  duodenal  ulcer,  diverti- 
culitis, carcinoma  coli,  renal  colic,  ovarian  and  tubal  disease, 
and  hypochondriasis.  Here  is  a characteristic  case: 

Case  11,  A medical  man,  aged  52,  consulted  me  for  an  abdominal 
‘ache’  of  many  years  standing.  The  pain  was  indicated  as  passing 
across  the  middle  of  the  abdomen  and  down  into  the  left  iliac  fossa. 
The  bowels  moved  twice  daily,  but  the  stools  were  commonly  hard 
and  fragmentary.  In  1027  and  1932  his  alimentary  tract  wa3  X-rayed 
with  negative  result.  Two  surgical  friends  declined  to  remove  his 
appendix.  At  first  he  used  to  lose  the  symptoms  on  a holiday.  He 
had  also  been  troubled  with  anal  pruritus,  from  which  a brother 
suffered  severely.  An  elder  sister  experienced  abdominal  symptoms 
like  his  own.  His  mother  and  some  maternal  cousins  had  had  eczema. 
Occasionally  he  had  severe  rectal  spasms,  both  by  day  and  by  night. 
Further  investigation  failed  to  reveal  any  evidence  or  organic  disease. 
There  were  good  reasons  for  considering  an  allergic  factor  in  view  of 
his  family  history.  Medicinal  and  dietary  measures  were  signally 
unsuccessful. 


Rectal  Neuroses 

Less  frequent  than  the  gastric  or  colonic  neuroses  the 
rectal  neuroses  are  capable  of  causing  greater  but  fortu- 
nately rarer  and  usually  briefer  pain  than  either.  In  the 
milder  forms  there  is  merely  a sensation  of  ‘a  Jump  in 
the  rectum’  or  of  something  to  be  evacuated  although  the 
bowel  is  empty.  These  might  be  described  as  cases  of  rectal 
‘globus’.  In  the  severe  type  the  patient  is  seized  with  an 
intense  pain  in  the  rectum  which  may  endure  from  five 
to  twenty  minutes  or  even  longer.  The  pain  is  described  as 
‘neuralgic’  or  ‘like  a bad  toothache’;  it  has  a sickening 


210  VISCERAL  NEUROSES 

quality  and  may  be  excruciating.  It  sometimes  gives  the 
impression  that  the  coccyx  is  being  forcibly  bent  inwards. 
These  rectal  crises  affect  both  sexes;  they  are  especially  apt 
to  occur  at  night  or  towards  the  early  hours  of  the  morning. 
In  none  of  my  cases  included  in  this  category  has  there  been 
any  evidence  of  tabes  dorsalis.  Fainting  sometimes  results 
from  the  pain,  which  is  presumably  due  to  an  intense  spasm 
of  the  powerful  local  sphincters.  Overwork  and  worry  have 
seemed  to  me  to  be  precipitating  causes.  Inflation  of  the 
rectum  with  air  may  bring  relief.  So  also  may  firm  sustained 
pressure,  inwards  and  upwards,  on  the  anal  sphincter. 

Vesical  Neuroses 

The  most  familiar  neuroses  of  the  bladder  are  the  enuresis 
of  childhood  and  the  inability,  so  common  in  nervous  men,  to 
micturate  in  public  or  in  the  doctor’s  presence  when  a speci- 
men of  urine  is  required.  In  the  first  relaxation  of  sphincters 
occurs  too  readily,  in  the  second  not  readily  enough. 

Sir  James  Paget  draws  a graphic  picture  of  a more 
exaggerated  form  of  nervous  difficulty,  in  which  complete 
retention  may  follow  upon  a nervous  and  ineffectual 
straining.  In  one  of  his  descriptions  a man,  who  had  once 
experienced  this  disability  while  out  walking  with  a lady 
friend,  declined  ever  to  go  walking  with  her  again  because 
he  knew  the  association  of  ideas  would  be  too  strong  for 
him  and  would  again  promote  a nervous  retention.  He  also 
mentions  the  case  of  a clergyman  who  always  passed  a 
catheter  before  going  into  the  pulpit  because  on  one  occasion, 
having  experienced  an  urgent  desire  to  micturate  during  a 
sermon,  he  found  himself  unable  to  perform  the  act  when  the 
sermon  was  over. 

Nervous  frequency,  commoner  in  women,  may  be  a great 
nuisance  and  often  follows  the  physically  induced  frequency 
of  cystitis. 

Nervous  incontinence  may  cause  misery  as  great  as 
nervous  retention,  and  I have  notes  of  one  young  married 
woman  who  suffered  the  combined  miseries  of  vaginismus, 
nervous  incontinence  of  urine,  and  nervous  diarrhoea,  and 
had  pain  both  in  bowel  and  in  bladder  after  evacuation.  Her 


VISCERAL  NEUROSES  211 

psychology  was  gravely  disturbed  and  her  nightmares  were 
all  in  connexion  with  lavatories. 

Cardiac  Neuroses 

I come  lastly  to  the  cardiac  neuroses,  a most  important 
group  on  account  of  the  fears  which  are  so  readily  engen- 
dered in  the  lay  mind  by  the  mere  suspicion  or  idea  of  heart 
disease.  With  these  cases  we  have  a very  special  respon- 
sibility. Much  harm  was  done  in  the  past  by  doctors  who 
labelled  functional  heart  disorder  as  cardiac  disease.  Equal 
harm  may  be  done  in  the  individual  case  by  a display  of  un- 
certainty as  to  the  nature  or  purport  of  cardiac  symptoms. 
As  a whole  the  profession  is  now  alive  to  the  compara- 
tive insignificance  of  many  murmurs,  of  extra-systoles,  and 
other  benign  arrhythmias  which  at  one  time  were  doubt- 
fully understood  and  often  too  seriously  regarded. 

Of  the  cardiac  neuroses  which  may  cause  the  most  dis- 
tressing symptoms  and  so  most  closely  simulate  organic 
disease,  I am  selecting  simple  paroxysmal  tachycardia  and 
the  nervous  anginas.  I shall  allow  a few  of  my  cases  to 
speak  for  themselves,  presenting  the  bare  facts,  for  brevity, 
without  indicating  the  considerable  effects  produced  by 
these  disturbances  on  mental  and  bodily  health. 

Case  12.  A man,  aged  09,  suffered  from  attacks  of  paroxysmal 
tachycardia  from  his  schooldays.  These  would  last  from  2 minutes 
to  5 hours,  and  always  started  and  ended  abruptly.  Bromides  dimin- 
ished them  and  lying  down  tended  to  stop  them.  Latterly  he  had 
also  developed  spasmodic  asthma. 

Case  13.  A man,  aged  62,  had  suffered  from  bouts  of  paroxysmal 
tachycardia  lasting  up  to  8 hours  for  a period  of  38  years.  The  pulse- 
rate  in  the  attacks  ranged  from  160  to  170.  He  was  able  to  ride  and 
golf  and  to  lead  an  active  life.  The  attacks  would  start  and  end 
abruptly,  and  were  commonly  preceded  by  a feeling  like  a tennis-ball 
below  the  left  ribs  ( ? colonic  globus).  He  himself  traced  a connexion 
between  the  state  of  his  bowel  and  the  cardiac  attacks. 

Case  14.  A woman,  aged  72,  had  been  troubled  for  20  years  by 
bouts  of  simple  paroxysmal  tachycardia,  starting  and  ending  abruptly 
and  lasting  many  hours.  Her  daughter  had  similar  attacks. 

Case  15.  A medical  student,  aged  21,  suffered  from  attacks  of 
paroxysmal  tachycardia  with  pulse-rate  varying  from  180  to  200  to 


212  VISCERAL  NEUROSES 

the  minute.  The  attacks  started  and  ended  abruptly  and  were  com- 
monly arrested  by  lying  down.  lie  also  had  asthma  and  was  a very 
bad  stammerer.  lie  continued  to  play  'rugger*  without  ill  effect. 

In  these  four  cases  we  have  exemplified  the  familial 
occurrence  of  paroxysmal  tachycardia ; associated  paroxys- 
mal neuroses — tachycardia  and  asthma — in  the  same  indi- 
vidual; and  finally,  in  Case  15,  ‘stammering’  in  no  less  than 
three  departments — speech,  heart,  and  bronchial  tree.  In 
each  case  long  continuation  of  the  cardiac  attacks  without 
physical  deterioration  or  mishap  was  manifest.  The  majority 
of  patients  with  a visceral  neurosis  are  afflicted  with  noso- 
phobia in  greater  or  less  degree.  Reassurance  alone  will 
never  cure  paroxysmal  tachycardia,  but  it  can  remove  un- 
necessary dread  and  contribute  to  general  well-being  and 
sometimes  a normal  way  of  life,  and  is  therefore  an  essential 
element  in  the  treatment  of  cases.  Care  may  be  necessary 
to  distinguish  simple  paroxysmal  tachycardia  from  such 
conditions  as  auricular  flutter  and  paroxysmal  fibrillation. 

Let  us  pass  finally  to  a consideration  of  certain  distressing 
attacks  which  simulate,  in  one  particular  or  another,  the 
dreaded  ‘breast-pang*  or  angina  pectoris.  There  are  cases 
in  which  only  careful  watching  over  long  periods,  with  or 
without  electro-cardiographic  studies,  can  make  the  distinc- 
tion between  the  graver  and  the  more  benign  disease.  The 
label  of  ‘pseudo-angina’  has  been  used  in  the  past  to  de- 
scribe the  nervous  and  more  innocent  condition,  but  since 
sternal  pain  with  arm-reference  and  angor  animi  may 
characterize  both  types,  and  the  pathology  of  symptoms,  if 
not  of  cause,  is  surely  identical,  and  since  in  both  the 
symptoms  are  real  enough,  the  nomenclature  is  surely 
undesirable.  A nervous  dyspepsia  which  simulates  peptic 
ulcer  is  not  a ‘pseudo-dyspepsia*.  It  were  better  to  speak 
of  nervous  or  vasomotor  angina  than  of  false  angina.  A 
number  of  these  cases  of  nervous  origin  fall  into  the  category 
of  the  vasovagal  attack,  as  defined  by  Gowers,  and  as  such 
I prefer  to  classify  them  both  for  purposes  of  clinical  study 
and  therapeutic  reassurance.  In  such  cases  there  is  com- 
monly a sense  of  substemal  or  praecordial  discomfort  or 
oppression  and  sometimes  of  very  real  pain.  Reference  to 


VISCERAL  NEUROSES  213 

tlie  neck  and  left  arm  also  occurs.  The  feeling  of  impending 
death,  which  probably  obtains  in  less  than  20  per  cent, 
of  cases  of  angina  of  effort  due  to  coronary  disease,  is 
present  in  the  majority  of  the  vasovagal  cases  and  often 
overshadows  the  physical  distress.  The  relationship  to 
effort  is  much  less  precise  than  in  the  organic  cases,  the 
duration  of  the  attacks  is  longer,  the  age-incidence  is 
younger,  and  female  cases  are  more  numerous.  A low  state 
of  physical  health  coupled  with  anxiety  of  mind  are  the 
most  evident  predisposing  causes. 

Pallor,  coldness,  and  fluctuating  blood-pressure,  and  a 
quick  or  very  slow  pulse  are  the  objective  features  of  the 
attack. 

Case  16.  A small,  highly  strung  woman,  aged  87,  and  a ‘martyr 
to  migraine’  lost  her  husband  suddenly.  She  suffered  great  grief  and 
was  referred  to  me  with  a complaint  of  attacks  of  praecordial  pain 
and  a sense  of  constriction  over  the  sternum,  coming  at  rest  or  with 
effort  and  often  waking  her  at  1 a.m.  and  lasting  for  as  long  ns  1 
hour.  It  had  become  impossible  for  her  to  push  her  child  aged  3 in 
the  pram.  Later  I saw  her  for  different  attacks  in  which  she  ‘felt 
dreadful’  and  ‘not  at  all  as  with  an  ordinary  faint’.  With  these  she 
became  very  cold  and  experienced  tightness  in  the  chest  and  her 
‘heart  felt  enormous’.  She  had  a low  blood-pressure  and  there  was 
no  evidence  of  cardiovascular  disease. 

Case  17.  A man,  aged  30,  who  had  suffered  from  anxieties  and 
prolonged  insomnia,  having  had  some  ‘nasty  sensations’  through 
the  day,  was  seized  with  palpitations  and  praecordial  pain  shortly 
after  getting  into  bed.  He  also  experienced  a sense  of  impending 
death.  His  heart  seemed  to  beat  forcibly  rather  than  fast.  There  was 
no  sign  of  cardiac  disease  and  his  blood-pressure  was  low,  and  his 
puise-rate  56.  I reassured  vigorously,  prescribed  bromides  with 
arsenic,  wine  with  his  dinner,  and  a good  holiday.  His  doctor  wrote 
5 years  later  to  say  that  be  had  remained  perfectly  well  ever  since. 

Summary  and  Treatment 

We  find,  then,  that  the  visceral  neuroses  affect  persons  and 
families  endowed,  usually,  with  the  neurotic  temperament 
in  greater  or  less  degree ; that  there  is,  as  many  of  my  case- 
notes  show,  a frequent  association  of  two  or  more  neuroses 
in  the  same  subject  or  the  same  family ; that  specificity  of 
cause  is  usually  lacking,  if  we  except  some  rare  instances 
of  idiosyncrasy  or  allergy;  but  that  influences  such  as 


214  VISCERAL  NEUROSES 

fatigue,  worry,  and  cold  may  all  be  contributory.  The 
disorders  are  in  no  sense  hysterical.  The  symptoms  may 
be  sufficiently  pronounced  to  suggest  organic  disease,  but 
intermittency,  periodicity,  the  mode  of  occurrence  of  the 
attacks,  the  precipitating  causes,  and  negative  physical 
studies  should  generally  serve  to  complete  the  differentiation. 
The  treatment  is  the  treatment  of  the  individual  patient. 
Explanation,  reassurance,  and  the  accepted  sedatives  and 
anti*spasmodics  including  bromides,  luminal,  and  bella- 
donna, all  play  their  part.  At  times  it  may  be  necessary  to 
take  a strong  stand  against  surgery  and  other  physical 
treatments  such  as  rest  in  bed  or  elaborate  dietetics  which 
may  have  been  injudiciously  prescribed.  Ever}'  endeavour 
should  be  made  to  improve  the  physiological  and  psycho- 
logical balance  by  a sensible  adjustment  of  conduct  and 
affairs.  By  such  means,  and  not  by  concentrating  our 
attentions  on  the  stammering  organ,  are  we  most  likely  to 
do  service’  to  patients  whose  sufferings  are  always  incon- 
venient and  sometimes  as  real  and  disabling  as  those  caused 
by  structural  disease. 

It  is  exactly  fifty  years  since  the  late  Sir  Clifford  Allbutt 
[3]  published  a brief  monograph,  based  on  his  Goulstonian 
Lectures  relating  to  the  visceral  neuroses.  The  lessons  which 
he  taught  have  never  been  so  widely  assimilated  as  they 
should  have  been,  and  his  little  book  is  all  too  little  known. 
We  have  advantages  in  the  shape  of  diagnostic  method  and 
appliances  which  he  did  not  possess  and  much  new  physio- 
logical and  psychological  knowledge  to  help  us  in  our  studies. 
If  we,  in  our  generation,  can  leam  to  leaven  our  newer 
methods  with  some  of  his  clinical  wisdom  and  humane 
philosophy,  the  next  fifty  years  should  add  much  to  our 
understanding  of  these  interesting  and  prevalent  disorders. 

REFERENCES 

1.  Paget,  Sib  James:  Clinical  Lectures  and  Essays.  London,  1870. 

2.  Pavxe,  W.  W.,  and  Pouetov,  E.  F.:  Quart.  Joum.  Med.,  1023, 

xvil.  53. 

3.  Alebdtt,  T.  Ceifford  : On  Visceral  Neuroses,  being  the  Goulstonian 

Lectures  on  Neuralgia  of  the  Stomach  and  Allied  Disorders,  Lon- 
don, 1884. 


XVI 


THE  NATURAL  HISTORY,  PROGNOSIS,  AND 

TREATMENT  OF  STAPHYLOCOCCAL  FEVER1 
It  was  customary  for  the  older  physicians,  untroubled  by  a 
plethora  of  laboratory  and  specialist  information,  to  study  in 
their  broad  outlines,  but  with  full  attention  to  clinical  detail, 
the  natural  history  of  the  diseases  which  confronted  them 
in  practice.  For  this  reason  their  descriptions,  although 
less  complete,  are  often  more  vivid  and  more  illuminating 
than  those  of  the  present  day.  Gull,  in  our  own  school, 
decrying  ‘a  narrow  pathology*,  was  insistent  on  the  value 
of  what  he  concisely  called  ‘the  general  view*,  and  his  wide 
comprehension,  sure  balance,  and  power  of  instruction  are 
evident  in  all  his  writings.  To-day  the  ‘general  view*  is 
rarely  taken,  the  journals  are  filled  with  separate  comments 
on  disease  from  the  pen  of  the  bacteriologist,  the  biochemist, 
and  the  medical  or  surgical  specialist,  and  under  the  influ- 
ence of  their  opinions,  often  too  limited  and  lacking  co- 
ordination, medical  philosophy  and  the  arts  of  prognosis 
and  treatment  have  not  uniformly  prospered.  There  must 
of  necessity  be  few  now  in  the  profession  who  are  so  widely 
instructed  and  so  constituted  that  they  can  take  a wholly 
unbiased  view  of  a disease ; who  can  read  at  once  the  effect 
upon  its  type  and  course  of  heredity,  environment,  and  per- 
sonality; who  can  gauge  the  proportionate  chances  of  infec- 
tion and  immunity;  who  can  visualize  behind  the  clinical 
image  the  intimate  processes  of  organ-  and  tissue-function ; 
who  can  assess  the  relative  importance  of  modem  objective 
methods  and  subjective  symptoms;  who,  applying  simul- 
taneously the  lessons  of  anatomy  and  morbid  anatomy,  of 
physiology  and  morbid  physiology,  can  think  both  surgi- 
cally and  medically.  The  subject  has  grown  too  vast. 
Nevertheless,  for  the  preservation  of  balance  it  is  essential 
that  the  ‘general  view’  be  taken  from  time  to  time,  and  that 
better  attempts  at  co-ordination  of  experience  be  made. 

1 This  and  the  two  ensuing  papers  were  introductory  to  Symposia  in  the 
Guy's  Hospital  Reports  (1030,  1031,  and  1032)  dealing  with  some  common 
infective  processes. 


21 G THE  NATURAL  HISTORY,  PROGNOSIS,  AND 

For  this  purpose  the  symposium,  whether  of  the  journal  or 
the  medical  society,  is  a convenient  method. 

In  selecting  for  review  the  local  and  general  consequences 
of  staphylococcal  invasions  we  are  selecting  a type  of 
disease  well  suited  for  consideration  by  this  method.  Staphy- 
lococcal infections  are  at  all  times  prevalent.  They  are  a 
part  of  the  daily  material  of  the  general  practitioner  and 
the  out-patient  department.  They  produce  complications 
which  fall  within  the  province  of  the  general  physician  and 
the  general  surgeon.  They  provide  problems  for  the  derma- 
tologist, the  bacteriologist,  and  other  specialists.  They 
create  important  difficulties  in  differential  diagnosis.  There 
is  much  uncertainty  as  to  the  value  of  the  immuno-thera- 
peutic  and  chemo-thcrapeutic  measures  often  employed  to 
combat  them.  While  infection  most  frequently  remains 
confined  to  the  skin  in  the  shape  of  boils  or  a carbuncle  it 
may  lead  to  a bacteriaemia  or  a septicaemia,  and  to  a group 
of  sequelae  so  varied  that  staphylococcal  fever  may  well 
be  regarded  as  one  of  the  most  protean  of  infective  diseases. 
It  is  usual  for  these  sequelae  to  be  separately  considered. 
How  much  less  satisfactory  would  our  understanding  of 
typhoid  fever  and  pneumonia  be  if  we  were  thus  to  sub- 
divide them  into  a number  of  separate  diseases  in  accor- 
dance with  their  local  and  special  types  of  complication. 
How  much  more  satisfactory  our  understanding  of  general 
staphylococcal  infection  becomes  when  we  regard  it,  in 
common  with  typhoid  and  pneumonia,  as  a specific  fever 
it  is  one  of  the  purposes  of  this  paper  to  show.  For  the  rest, 
the  remarks  which  follow  are  intended  as  an  introduction 
to  contributions  by  my  colleagues  in  exposition  of  surgical 
and  other  aspects  of  the  disease. 

Under  the  title  of  staphylococcal  fever  I shall  include 
all  the  immediate  febrile  consequences,  together  with  their 
metastatic  accompaniments,  which  may  from  time  to  time 
complicate  a boil  or  carbuncle. 

With  illustrations  from  a small  series  of  cases  personally 
observed  I shall  endeavour  to  depict  the  natural  history  of 
staphylococcal  fever,  to  consider  in  brief  the  difficulties  in 
diagnosis  and  differential  diognosb  which  it  may  present, 


TREATMENT  OF  STAFHYLOCOCCAI,  FEVER  217 
and  to  discuss  prognosis  and  the  merits  of  the  therapeutic 
methods  nosv  in  vogue. 

Of  the  general  pathology  of  diffuse  infections  with  Staphy- 
lococcus aureus  we  may  say  firstly  that  they  have,  in  nearly 
all  cases,  a primary  skin  focus.  Mucosal  invasions  may 
occur,  but  this  is  less  certainly  established.  The  focus  may 
be  in  the  guise  of  a pimple,  a stye,  a solitary  boil,  a wide- 
spread furunculosis,  a carbuncle,  or  an  infected  wound  or 
abrasion.  From  time  to  time,  and  more  commonly  than  is 
generally  appreciated  (although  fortunately  still  in  a minor- 
ity of  cases),  fever  follows  of  short  or  long  duration.  In  a 
considerable  proportion  of  all  cases  of  staphylococcal  fever 
there  is  a true  bacteriaemia  or  septicaemia  with,  or  only 
very  occasionally  without,  multiple  metastases  or  a solitary 
metastasis. 

Staphylococcal  fever  is  a disease  more  particularly  of 
childhood  and  young  adult  life,  but  there  are  strikingly 
different  liabilities  in  the  different  age-periods.  In  children 
metastasis  in  bone,  leading  to  acute  osteomyelitis,  is  the 
usual  sequel.  A long  bone  is  the  site  of  election,  or  more 
rarely  some  part  of  the  pelvic  girdle.  With  prompt  and  ade- 
quate treatment  the  disease  may  here  become  arrested.  In 
unfavourable  cases  there  is  a continuance  of  the  original 
septicaemia  or  a secondary  septicaemia  develops  with  dis- 
semination of  multiple  small  abscesses  into  the  kidneys,  the 
heart,  and  the  lungs.  In  adults  osteomyelitis  is  rare  and  a 
boil  or  carbuncle  of  the  kidney  with  resulting  perinephritis 
or  perinephric  abscess  is  the  more  usual  sequel.  Some 
authors  have  referred  to  staphylococcal  perinephritis  as 
though  it  could  occur  by  direct  metastasis  into  the  peri-renal 
cellular  tissues.  My  experience  suggests  that  it  is  invariably 
secondary  to  a sub-capsular  renal  boil  or  carbuncle  (see 
Ryle,  J.  A.,  Brit.  Joum.  of  Urology , 1938,  x.  337).  Without 
serious  pyaemic  manifestations  metastases  also  occur  in 
the  prostate,  or  in  muscle.  In  the  graver  cases  with  septic- 
aemia multiple  lung  abscesses  are  common.  Abscesses  in 
the  skin  are  not  infrequent.  A solitary  focus  in  the  tibia 
may  become  imprisoned  and  lead  to  a chronic  Brodie's 
abscess.  Rarer  sites  for  a secondary  abscess  are  the  brain 


218  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
or  a vertebra.  Both  in  children  and  in  adults  it  is  clear 
from  clinical  histories  and  a knowledge  of  environment 
and  antecedents  that  staphylococcal  fever,  whether  benign 
or  malign,  is  infrequent  under  good  general  conditions  of 
life  and  health.  Osteomyelitis  is  more  a disease  of  the 
city  hospital  than  of  private  practice  among  the  comfort- 
ably situated ; perinephric  abscess  or  septicaemia  in  an  adult 
is  commonly  the  end-result  of  lowered  -vitality  through 
recent  illness  or  overwork.  The  well-known  occurrence  in 
some  persons  of  furunculosis  relapsing  over  long  periods 
has  suggested  that  natural  immunity  may  be  so  far  lost  that 
an  actually  increased  sensitiveness  to  the  staphylococcus 
becomes  established,  such  a sensitiveness  being  regarded 
by  some  as  akin  to  the  specific  types  of  sensitiveness  shown 
in  the  allergic  disorders.  Even  a serious  staphylococcal 
illness  successfully  weathered  docs  not  necessarily  confer 
lasting  immunity  (vide  Cases  1, 7,  and  9).  A small  focus  may 
also  lie  latent  for  months  or  years  and  then  give  rise  to  a 
fresh  generalized  or  metastatic  infection  (Case  9?).  I have 
also  seen,  on  more  than  one  occasion,  a staphylococcal  in- 
fection pave  the  way  for  a streptococcal  septicaemia. 

In  diabetes  it  has  long  been  recognized  that  there  is  an 
increased  liability  to  boils  and  carbuncles.  On  the  basis  of 
this  knowledge  it  has  been  supposed  that,  without  diabetes, 
an  excessive  consumption  of  sugar  and  starch  may  predis- 
pose to  staphylococcal  infection. 

The  terms  bactcriaemia  and  septicaemia  (or  pyaemia)  are 
employed  with  special  reason.  In  each  case  it  is  to  be  in- 
ferred, from  the  fact  that  distant  metastatic  infection  occurs, 
that  organisms  have  found  their  way  into  and  been  dis- 
seminated by  the  blood-stream.  In  bactcriacmia  the  stage 
of  transit  has  been  comparatively  unev  entful  and  unaccom- 
panied by  such  evidences  of  grave  activity  as  repeated 
rigors  or  high  swinging  pyrexia.  The  cases  are  commonly 
seen  first  or  diagnosed  first  in  the  stage  when  local  symp- 
toms of  an  abscess  have  developed  and  the  opportunity  of 
proving  a stage  of  bacteriaemia  by  blood  culture  has  passed ; 
the  fever  terminates  when  the  abscess  is  drained.  In  septic- 
aemia or  pyaemia  an  initial  rigor  or  recurrent  rigors,  pro- 


TREATMENT  OP  STAPHYLOCOCCAL  FEVER  210 
fuse  sweats,  high  sustained  or  swinging  pyrexia,  sometimes 
continuing  for  many  weeks,  and  multiple  abscesses  announce 
only  too  plainly  to  the  clinician  what  blood  culture  may 
readily  confirm,  namely,  the  presence  of  thriving  organisms 
in  the  circulating  blood.  This  distinction  between  a bacteri- 
aemia  and  a septicaemia  may  seem  arbitrary,  but  it  is 
clinically  important.  It  is  perhaps  a question  of  degree  of 
infection,  or  it  may  depend  in  some  instances  on  the  readi- 
ness W’ith  which  certain  tissues  show  themselves  capable  of 
forming  a spontaneous  fixation  abscess.  We  can  at  present 
do  no  more  than  guess  at  the  relative  determining  influence 
of  the  numerical  factor  on  the  part  of  the  invaders  and  the 
particular  qualities  of  the  defence.  We  know  that  some 
constitutional  types  support  infection  less  well  than  others. 

The  cases  (1-9)  described  hereunder  have  been  taken 
from  my  private  case-notes  in  chronological  order  and  with- 
out selection.  Case  10,  which  was  referred  to  me  at  my  Out- 
Patients  and  was  later  admitted  to  Clinical  Ward  under  the 
care  of  Dr.  E.  P.  Poulton,  is  included  as  an  example  of 
ambulant  staphylococcal  fever  with  metastatic  abscesses 
in  muscle,  tonsil,  and  skin. 

Case  1.  Furunculosis.  Staphylococcal  fever  ( bacteriaemia ).  Perine- 
phric abscess.  Recovery.  I was  consulted  on  20  September  1921  by  a 
newly  qualified  medical  man,  aged  25,  then  holding  a house-appoint- 
ment. For  several  weeks  he  had  been  feeling  unfit,  hut  had  been 
playing  football  for  the  hospital.  He  had  a slight  cough.  A few 
mornings  previously  he  had  wakened  with  blood  in  his  mouth  and 
on  the  pillow.  His  temperature  was  100.  There  were  no  physical 
signs  of  lung  disease  and  no  tubercle  bacilli  were  found  in  the  sputum. 
He  had  recently  had  boils  and  a slight  antral  infection.  He  got  well 
and  again  played  football.  On  1 December  1921  I was  asked  to  see 
him  in  his  own  home,  where  he  had  been  lying  for  a fortnight  under 
suspicion  of  paratyphoid  fever.  His  illness  had  started  with  a chill. 
He  had  then  run  a remittent  pyrexia  with  temperatures  ranging 
between  101  and  lOi.  There  bed  been  an  occasional  sweat  end  a 
slight  cough.  Bowels  normal.  Tongue  fairly  clean.  No  splenic 
tumour.  No  rose-spots.  No  T.B.  in  sputum.  Negative  agglutinations 
against  organisms  of  the  typhoid  group.  For  4 days  past  he  had  had 
pain  in  the  left  lower  chest  and  left  loin  on  coughing  or  deep  breathing 
or  turning  over  in  bed.  There  was  tenderness  and  contraction  of  the 
rectus  on  palpating  under  the  left  rib  margin.  Air-entry  was  deficient 
at  the  left  base,  but  there  was  no  pleuritic  friction.  There  was  a very 


220  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
tender  spot  over  the  last  rib  and  in  the  last  space  on  the  left  and  very 
alight  tumefaction  of  the  loin.  Leucocyte  count  20,000  cells  per  c.mm. 
Urine  normal.  A provisional  diagnosis  of  perinephric  abscess  was 
made  and  he  was  sent  into  hospital.  In  the  s\ard  his  temperature 
came  down  in  step-ladder  fashion,  his  leucocytes  fell  to  15,000  per 
c.mm.,  but  loin  tenderness  and  impaired  movement  of  the  left 
diaphragm  persisted.  On  C December  1021  the  temperature  was 
normal,  but  there  was  definite  swelling  in  the  loin.  The  signs  of  lung 
compression  reached  the  angle  of  the  left  scapula,  hut  no  fluid  was 
obtained  on  needling.  Mr.  R.  P.  Rowlands  opened  a walled  peri- 
nephric abscess  of  the  size  of  a golf-ball  in  the  left  post-renal  space. 
The  massive  collapse  of  the  left  lower  lobe  persisted  for  some  time. 
Otherwise  recovery  was  uneventful.  I saw  him  again  on  18  March 
1022  for  boils  on  the  neck  and  chest  following  a follicular  tonsillitis. 
Since  then  he  has  kept  well  m a busy  practice. 

Case  2.  Furuncle.  Staphylococcal  fever  (septicaemia).  Renal,  cere- 
bral, and  lung  abscesses.  Death.  A man,  aged  35,  of  rather  fat  un- 
healthy type,  was  taken  ill  with  a cold  then  prevalent  in  his  house  on 
25  October  1023.  He  had  remained  feverish  up  to  the  day  of  my  visit 
on  3 November  1023,  when  Ids  temperature  reached  104.  On 
29  October  1023  he  had  drawn  the  attention  of  his  doctor,  the  late 
Dr,  E.  Hardenberg,  to  a boil  on  the  left  wrist  wluch  liad  already  been 
there  some  days.  He  complained  of  pain  low  in  the  left  chest  aggra- 
vated by  deep  breathing  or  rolling  on  to  his  right  side.  His  tongue 
was  furred.  He  looked  ill  and  limp.  There  was  an  area  of  exquisite 
tenderness  no  larger  tlian  a florin  immediately  below  the  12th  rib 
on  the  left  side.  Urine  normal.  Leucocyte  count  14,000  per  c.mm. 
A Widal  test  had  already  been  performed  with  negative  result.  On 
5 November  he  developed  right-sided  pleuritic  pain  and  began  to 
cough  up  sputum,  at  first  rusty,  then  sanguineo-purulcnt.  On 
10  November  temperature  swinging;  pulse  03-100;  respirations  30- 
40.  Left  flank  signs  subsiding.  Impaired  note  at  right  base  'with 
distant  tubular  breathing.  Leucocytes  13,000  per  c.mm.  On 
10  November  after  a definite  improvement  with  a drop  in  the  tem- 
perature and  diminishing  signs  at  the  right  lung-base,  be  developed 
a left  femoral  thrombosis.  In  spite  of  this  his  general  condition 
appeared  good  and  his  mental  outlook  was  more  cheerful.  A week 
later  he  liad  abdominal  distension,  became  unconscious,  anddeveloped 
a squint  and  slight  head  retraction;  his  temperature  rose  to  103 
and  he  died,  presumably  from  a cerebral  abscess. 

It  is  noteworthy  that  this  man  was  of  unhealthy  type  and 
that  he  never  showed  a good  leucocytic  response.  Neverthe- 
less, I have  since  wondered  whether  early  operation  on  the 
left  kidney  or  drainage  of  the  perinephric  tissues  might  have 
saved  his  life. 


TREATMENT  OF  STAPHYLOCOCCAL  FEVER  221 
Cass;  3.  Furuncle.  Staphylococcal /ever  { septicaemia ).  Abscesses  in 
kidney,  lung,  skin.  Tlecovery.  This  was  the  case  of  a medical  man 


Case  8 (1st  Week) 


aged  22  (seen  2 July  1927  in  consultation  with  Dr.  Richard  Clarke  of 
Bristol),  who  6 weeks  previously  and  10  days  after  the  healing  of  an 
obstinate  boil  on  the  chin,  developed  high  pyrexia  with  left  loin  dis- 
comfort. Staphylococcal  septicaemia  was  soon  afterwards  diagnosed 


222  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
and  confirmed  by  blood  culture.  Within  a fortnight  of  the  onset 
the  left  loin  was  incised  on  account  of  tenderness,  but  the  kidney 
was  not  apparently  explored  and  no  pus  was  found.  There  was  a 
Icucocytosis  varying  from  18  to  20  thousand  cells  per  canm.  On 
22  June  the  loin  wound  had  been  reopened  on  the  advice  of  Dr.  A.  F. 
Hurst  and  some  pus  found.  A week  later  he  became  desperately  ill 
with  signs  of  effusion  in  the  left  chest.  Blood-stained  fluid  was  ob- 
tained with  the  needle  and  the  effusion  was  drained  with  a catheter 
detween  the  ribs.  On  a few  occasions  he  had  coughed  up  muco-pus. 


When  I saw  him  he  had  developed  se\  eral  small  deep  abscesses  on 
the  trunk,  over  both  breasts  and  the  back.  He  looked  very  ill,  was 
hectic  and  wasted  and  tremulous  like  a third-week  typhoid  case. 
After  my  visit  he  coughed  up  blood  and  pus  on  several  occasions 
and  had  patchy  signs  in  both  lungs.  During  this  anxious  phase  there 
were  rigors.  Nevertheless  he  weathered  the  storm.  His  temperature 
became  normal  on  15  August,  12  weeks  after  the  onset  of  his  illness, 
and  his  restoration  to  health  was  complete.  The  specimen  charts 
arc  taken  from  the  first,  fifth,  and  ninth  weeks  of  observation.  In 
the  earlier  stages  he  was  given  injections  of  inercurochromc,  which 
gave  him  a slight  enteritis  and  in  his  opinion  brought  no  benefit. 

Cask  4.  Staphylococcal  fever  { septicaemia ).  Lung  abscesses.  Osteo- 
myelitis of  femur.  Recovery.  On  SO  October  1025  I saw,  in  consulta- 
tion with  Dr.  W.  O’Brien  of  Brockley,  a well-built,  intelligent  boy, 
aged  1 G,  who  had  been  taken  ill  4 days  previously  with  upper  abdomi- 
nal pain  aggravated  by  breathing.  lie  had  a high  fever,  looked 
gravely  ill,  was  breathing  fast,  and  there  were  signs  of  right  basal 
pleurisy.  On  the  previous  night  he  had  also  developed  great  pain  in 
the  lower  portion  of  the  right  femur.  The  thigh  was  swollen  here  and 
exquisitely  tender.  The  knee-joint  was  not  involved.  He  was  ad- 


TREATMENT  OF  STAPHYLOCOCCAL  FEVER  2*23 
mitted  to  Guy’s  under  the  care  of  Mr.  F.  J.  Steward.  An  operation 
was  performed  for  osteomyelitis  of  the  femur.  Blood  cultures  grew 
Staphylococcus  aureus.  For  many  weeks  this  boy  was  desperately  ill. 
He  developed  many  lung  abscesses,  especially  in  the  left  upper  lobe, 
with  considerable  bright  haemoptyses.  Fluid  aspirated  from  the  left 
pleural  sac  grew  Staphylococcus  aureus.  At  one  time  and  another  in 
the  early  stages  he  was  given  mercurochrome  and  vaccines  without 
the  slightest  evidence  of  any  good  effect  on  his  symptoms  or  pyrexia! 
curve.  He  eventually  made  a good  recovery,  but  was  re-admitted 
later  for  sequestrectomy. 

Case  5.  Furunculosis.  Staphylococcal  fever  (septicaemia).  Recovery. 
On  3 February  1920  I saw,  in  consultation  with  Dr.  A.  E.  Gow  and 
Dr.  James  Rannic,  a dental  surgeon,  aged  34.  For  2 or  3 years  this 
patient  had  been  unfit,  originally  with  a carbuncle  and  since  then 
with  recurrent  furunculosis.  During  the  past  month  he  had  had  a 
troublesome  boil  on  the  right  thigh.  A fortnight  previously  he  had 
had  influenza  with  laryngitis.  A few  days  later  he  developed  a cough 
with  patch}'  pneumonic  signs  at  the  right  base.  His  temperature  had 
remained  high  (102-5),  pulse-rate  rarely  above  90,  respirations  20. 
There  had  been  some  purulent  sputum,  occasionally  tinged  with 
blood,  from  which  Staphylococcus  aureus  was  grown.  There  had  been 
one  rigor  at  the  beginning  of  the  illness  and  one  in  the  past  24  hours. 
He  had  been  treated  initially  with  a pneumococcus  immunogen.  Sub- 
sequently he  had  had  two  doses  of  a vaccine  and  an  intravenous 
injection  of  mercurochrome.  None  of  these  measures  had  in  any  way 
influenced  his  symptoms  or  his  temperature  curve.  He  was  a dark, 
stocky  type  of  man  and  well  covered.  He  ‘looked  septic’  and  was 
clearly  very  ill.  There  was  a recent  stye  on  the  right  lower  eyelid. 
The  spleen  was  not  palpably  enlarged.  The  chest  was  clear  except  for 
rhonchus  at  the  angle  of  the  right  scapula.  Staphylococcal  septicae- 
mia was  diagnosed,  and  this  was  confirmed  by  blood-culture.  Symp- 
tomatic treatment  with  a copious  fluid  intake  was  advised.  I next  saw 
him  on  15  February.  High  pyrexia  had  continued  and  there  was  a 
duller  note  at  the  right  base.  That  morning  he  had  been  seized  with 
sudden  severe  pain  in  the  right  upper  chest  in  front  together  with 
great  difficulty  in  breathing.  The  liver  dullness  was  seemingly 
diminished  and  I queried  a small  anterior  pneumothorax.  There  was 
a wide  band  of  cutaneous  hyperalgesia  corresponding  with  three  or 
four  of  the  upper  dorsal  roots.  I did  not  see  the  patient  again,  but 
I learned  that  the  illness  continued  uneventfully  until  he  developed 
an  acute  streptococcal  tonsillitis  a week  or  two  later,  for  which  he  was 
given  antistreptococcic  serum.  He  then  made  a complete  recovery. 

Case  G.  Staphylococcal  fever  (septicaemia).  Pulmonary  abscesses. 
Blood-stained  pleuritic  effusion.  Recovery.  A man,  aged  28  (seen  in 
consultation  with  Dr.  A.  J.  Williamson  of  Watford,  13  April  1929), 
gave  a history  of  an  ‘ordinary  dull*  3 or  4 weeks  previously.  He 


22  V THE  NATURAL  HISTORY,  PROGNOSIS,  AND 

remained  at  work  for  several  days,  but  then  became  more  seriously 
ill.  On  3 April  he  was  admitted  to  hospital  with  high  fever,  sustained 
at  first,  but  swinging  latterly.  With  this  he  had  profuse  night-sweats, 
and  cough  with  nummular,  purulent  sputum  just  beginning  to  be 
streaked  with  blood.  Pleuritic  signs  had  appeared  at  the  right  base 
on  31  April,  but  only  a small  quantity  of  clear  fluid  was  obtained  on 
needling.  A provisional  diagnosis  of  acute  pneumonic  pulmonary 
tubercle  had  been  made,  but  no  bacilli  were  reported  in  the  sputum. 
The  patient  looked  to  me  not  phthisical,  but  septicacraic.  He  was 
muscular,  well-covered,  bright-eyed,  and  still  alert  and  vigorous. 
The  tongue  was  fairly  moist.  There  was  one  large  yellow  follicle  on 
the  right  tonsil.  He  gave  no  history  of  boils  or  cutaneous  sepsis. 
There  was  no  loin  tenderness.  There  were  signs  of  a large  effusion 
in  the  right  chest  which  I needled,  withdrawing  intimately  blood- 
stained serous  fluid.  Later  nccdlings  of  the  chest  gave  similar  slightly 
turbid  blood-stained  fluid.  Cultivations  both  from  the  fluid  and  from 
the  blood  grew  Staphylococcus  aureus.  The  patient  made  a complete 
recovery,  interrupted  only  by  a small  saphenous  thrombosis. 

Case  7.  Furunculosis.  Staphylococcal /ever  (baclcriaemia).  Perine- 
phritis. Recovery.  A medical  man,  aged  42,  who  had  had  o staphy- 
lococcal infection  with  prostatie  abscess  during  his  war-serviec,  had 
some  small  boils  in  June  1020.  At  the  end  of  that  month  he  had  a 
solitary  rigor  and  thereafter  was  laid  up  with  a swinging  temperature 
for  2 weeks.  The  temperature  then  subsided,  and  he  got  about  again 
but  remained  unwell,  with  symptoms  and  signs  of  irritation  of  the  left 
psoas  muscle.  He  had  slight  scoliosis  and  was  compelled  to  walk  in 
a constrained,  slightly  stooping  attitude,  and  could  not  easily  bring 
the  heel  of  the  left  foot  to  the  ground.  Ilis  tongue  was  brown  and  he 
looked  ‘poisoned*.  There  was  tenderness  and  ‘guarding’  in  the  left 
loin.  At  an  earlier  stage  he  had  had  pain  and  tenderness  in  the  left 
iliac  fossa,  and  he  remarked  that  ‘he  was  sure  he  would  liave  had  his 
appendix  removed  if  the  pain  had  been  on  the  right’.  There  was 
slight  impairment  of  respiratory  movement  and  percussion  note  at 
the  left  base.  Mr.  E.  C.  Hughes,  with  whom  I saw  him  in  consulta- 
tion, operated  on  1 August  1929,  incising  the  loin,  where  he  found 
hard,  oedematous,  peri-renal  fat,  but  no  actual  pus.  A drainage  tube 
was  inserted  and  through  this  a very  small  amount  of  scro-san- 
guineous  fluid  was  later  discharged.  A complete  recovery  followed. 

Case  8.  Furunculosis.  Staphylococcal  fever  (bacteriaemia).  Perine- 
phric abscess » Recovery.  The  patient,  seen  10  Januaiy  1030  in  con- 
sultation with  Dr.  C.  H.  Hall  and  Mr.  A.  S.  Gough  of  Watford,  was  a 
robust  young  man  and  a keen  footballer.  Between  20  December  1029 
and  23  December  he  was  apparently  suffering  from  slight  chills,  as  ‘he 
kept  asking  to  have  the  windows  shut*.  He  then  developed  pain  in 
the  left  loin  passing  down  the  left  leg,  and  was  found  to  have  some 
pyrexia.  After  a transient  improvement  he  became  worse  and  was 


TREATMENT  OF  STAPHYLOCOCCAL  FEVER  225 
sent  into  a nursing-home,  where  he  continued  to  complain  of  pain 
in  the  left  loin  and  had  frequent  night-sweats.  His  temperature  had 
been  swinging  between  the  base-line  and  102  or  103.  His  pulse-rate, 
normally  60,  had  not  exceeded  70  to  the  minute.  Turning  over  in 
bed,  a sudden  deep  breath,  and  stretching  out  the  left  leg  all  aggra- 
vated the  pain.  There  was  guarding  of  the  left  loin  muscles,  slight 
tumefaction,  and  a single  spot  of  exquisite  tenderness  below  the  last 
rib.  There  was  impairment  of  movement  and  entry  at  the  left  base. 
There  was  n well-marked  Jeucocytosis  (20,000  cells  per  c.irnn.).  A 
perinephric  abscess  was  diagnosed  and  drained  by  Mr.  Gough  the 
next  day.  A satisfactory  recovery  followed. 

Case  9.  Staphylococcal  fever  ( septicaemia ) with  lung  abscesses  and 
right  perinephric  abscess.  Recovery.  Four  years  later  recurrence  of  inf  ec- 
tion  in  the  left  kidney  with  perinephric  abscess.  A young  medical  man 
was  troubled  in  1923  by  symptoms  relating  to  the  left  hip.  Varying 
opinions,  medical  and  surgical,  were  given,  and  tuberculosis  of  the 
joint  was  discussed.  No  final  diagnosis  was  made  and  the  symptoms 
eventually  departed.  Between  that  year  and  1026  he  had  a bad  car- 
buncle on  the  neck.  In  1 926  he  was  in  hospital  for  several  months  for 
a very  serious  illness  with  haemoptyses,  pulmonary  signs,  and  sweats. 
For  a time  he  was  thought  to  have  pulmonary  tuberculosis.  Even- 
tually a large  perinephric  abscess  on  the  right  side  was  found  and 
drained.  He  made  a complete  recovery  and  returned  to  practice. 
Early  in  February  1930  he  developed  pain  in  the  left  loin,  of  no  great 
severity  at  first,  and  with  it  pyrexia.  A fortnight  later  a left  peri- 
nephric abscess  localized  and  was  operated  on  by  Mr.  F.  J.  Steward. 
Staphylococcus  aureus  was  grown  from  the  pus.  The  pyrexia,  however, 
did  not  subside  and  he  continued  to  run  a high  swinging  temperature 
with  night-sweats.  His  urine  was  found  to  contain  red  cells,  pus  cells, 
and  a few  granular  casts ; staphylococci  were  also  grown.  There  was 
slight  pain  at  the  end  of  micturition.  In  spite  of  the  high  temperature, 
which  varied  between  102  and  104,  the  pulse  remained  proportion- 
ately slow,  the  tongue  was  clean,  and  food  and  fluids  were  partaken  of 
freely.  For  a time  there  were  signs  of  diaphragmatic  inhibition  with 
lung  compression  at  the  left  base,  but  these  had  disappeared  when 
I saw  him  for  the  first  time  in  consultation  with  Dr.  A.  H.  Douthwaite 
and  Dr.  D.  Whitlock  on  25  March  1930.  There  were  no  signs  of  local 
infection  elsewhere  than  in  the  left  loin.  Prostate  gland  slightly 
tender  but  not  enlarged.  There  were  no  clinical  signs  pointing  to  a 
general  septicaemia  and  blood  cultivations  liad  been  repeatedly  nega- 
tive. The  urinary  findings  and  symptoms  taken  in  conjunction  with 
the  fever  clearly  suggested  that  the  whole  of  the  renal  sepsis  had  not 
been  ‘tapped*  in  the  course  of  draining  the  perinephric  abscess. 
Mercurochrome  had  been  given  without  apparent  benefit.  After  a 
long  illness  recovery  was  complete. 

This  is  the  only  case  in  my  experience  in  which  such  urinary  find- 

Q 


220  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
ings  were  present.  As  a rule  the  urine  in  perinephritis  is  free  from 
blood,  pus,  albumen,  and  casts.  From  this  it  might  be  argued  that 
the  kidney  is  not  primarily  involved,  but  it  may  equally  be  advanced 
as  evidence  that  the  renal  abscesses  are  generally  small  and  localized 
in  the  cortical  zone,  and  that  they  tend  to  erupt  spontaneously  on  the 
surface  of  the  kidney.  There  was  no  Iiistory  of  any  recent  cutaneous 
lesion.  Scanning  the  history  of  this  case  it  is  interesting  to  speculate 
(1)  whether  there  had  becna  focus  lying  dormant  ever  since  the  scptic- 
aemic  illness  in  1020,  and  (2)  whether  the  suspected  left  hip-joint 
disease  in  1023  may  have  been  due  to  an  undiscovered  staphylococcal 
infection  of  bone  or  soft  tissues  in  that  neighbourhood. 

Cask  10.  Infected  abrasions.  Staphylococcal  fever  (bacteriaemia). 
Abscesses  in  skin,  muscle,  and  a tonsil.  A boy,  aged  18,  was  referred  to 
my  Out-Patients  by  Dr.  II.  E.  Rattle  on  28  February  1029  for  small 
tumours  of  the  back,  right  forearm,  left  tliigh,  and  left  buttock.  The 
first  three  were  superficial  and  not  tender  and  were  situated  in  the 
dermis.  The  fourth  was  deep  in  the  muscle  and  tender.  Cultures  from 
all  of  them  grew  Staphylococcus  aureus.  A culture  from  a tonsillar 
focus  grew  Staphylococcus  aureus  and  a streptococcus.  Blood  cultures 
remained  sterile.  The  boy  complained  of  no  general  feelings  of  Illness, 
but  was  found  to  be  running  a temperature  with  morning  intermis- 
sions and  evening  rise.  The  spleen  was  palpable.  Leucocyte  count 
10,000  per  c.mm.  For  3 weeks  he  had  been  suffering  from  septic 
abrasions  over  both  heels.  The  large  nbsecss  in  the  buttock  was 
drained.  The  temperature  did  not  settle  completely  for  a month. 

Discussion 

From  these  cases  of  staphylococcal  fever  some  instructive 
conclusions  in  respect  of  aetiology,  differential  diagnosis, 
prognosis,  and  treatment  may  be  drawn. 

Aetiology.  In  this  small  series  all  ten  cases  were  males;  I 
have  a strong  impression  from  cases  seen  elsewhere  and 
subsequently  that  the  incidence  of  staphylococcal  fever  is 
higher  in  the  male  sex.  Their  ages  were  between  thirteen 
and  fort y- two  years.  The  influence  of  preceding  ill  health  is 
suggested  by  the  histories  of  Cases  1,2,  and  5.  Cases  3, 7,  and 
9 were  in  overworked  medical  men.  Case  10  was  that  of  a 
boy  in  poor  circumstances  and  not  well  cared  for.  In  seven 
of  the  ten  cases  there  was  a clear  account  of  a primary  focus 
in  the  shape  of  a boil  or  other  cutaneous  sepsis. 

Differential  diagnosis.  A diagnosis  of  typhoid  group  infec- 
tion had  been  seriously  considered  during  the  initial  fever 
in  Cases  1 and  2.  The  possibility  of  pulmonary  tuberculosis 


TREATMENT  OF  STAPHYLOCOCCAL  FEVER  227 
was  discussed  in  Cases  1 and  6.  In  Case  9 pulmonary  tuber- 
culosis was  the  initial  diagnosis  in  a previous  attack  of 
severe  septicaemic  staphylococcal  fever.  Case  5 was  for  a 
short  time  treated  as  an  influenzal  pneumonia.  Case  7.  a 
medical  man,  had  a scoliosis  and  a painful  and  difficult  gait 
which,  with  an  inadequate  history,  might  have  led  to  a 
diagnosis  of  spinal  or  hip  disease.  A girl  recently  under  the 
care  of  Dr.  Hurst  and  myself  in  Clinical  Ward  with  peri- 
nephric abscess  had  attended  an  Orthopaedic  Out-Patient 
Department  as  a spinal  case  for  many  months.  Case  7 also 
confessed  that  his  abdominal  pain  in  an  earlier  stage,  had  it 
been  on  the  right  side,  would  almost  certainly  have  led  to 
an  appendicectomy. 

The  differentiation  from  typhoid  fever  depends  upon  the 
discovery  of  a present  or  recent  primary  focus  of  infection, 
the  absence  of  conspicuous  splenic  enlargement,  rose-spots, 
and  intestinal  symptoms,  and  the  presence  from  the  begin- 
ning of  a leucocytosis.  The  pulse  in  staphylococcal  fever  is 
frequently  slow  in  proportion  to  the  temperature,  a small 
point  which  may  lend  support  to  a suspicion  of  typhoid 
infection.  Haemoptyses  and  night-sweats  and  pleuritic 
effusion  may  very  well  suggest  a diagnosis  of  acute  pulmo- 
nary tuberculosis,  but  again  the  leucocyte  count,  the  history, 
and  sputum  examinations  should  help  to  decide  the  issue, 
I should  like  to  emphasize  the  frequency  and  diagnostic 
significance  of  sweats  in  staphylococcal  fever,  whether  due 
to  a focal  or  general  infection.  After  tuberculosis  and  infec- 
tive endocarditis  it  should  be  regarded  as  one  of  the  most 
important  of  the  ‘sweating’  fevers.  The  diagnosis  from 
streptococcal  fever  can  commonly  be  made  on  the  history 
and  particularly  on  the  nature  and  site  of  the  initial  lesion. 
In  streptococcal  septicaemia  rigor  is  more  common  and 
sweating  less  common ; glossitis,  diarrhoea,  rapidly  develop- 
ing anaemia,  and  splenic  enlargement  mark  the  infections 
with  a haemolytic  streptococcus,  and  are  absent  in  staphy- 
lococcal fever.  The  streptococcus  selects  the  joints,  the 
pleura,  and  the  pericardium  for  its  metastatic  infections  and 
does  not  produce  the  multiple  small  abscesses  in  the  soft 
tissues  and  organs  named  above  as  favoured  by  the  staphy- 


228  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
lococcus.  A rapid  pulse  from  the  beginning  is  more  frequent 
in  streptococcal  than  in  staphylococcal  fever. 

Prognosis.  With  ever}'  case  of  septic  fever  there  is  a neces- 
sary sense  of  alarm,  but  too  often  alarm  verges  upon  panic 
or  despair.  It  is  true  that  certain  septicaemias,  and  notably 
those  fulminant  streptococcic  infections  to  which  the  sur- 
geon, the  pathologist,  and  the  puerperal  woman  fall  victim, 
may  pass  almost  immediately  beyond  human  control  in  the 
absence  and  sometimes  in  spite  of  prompt  chemotherapy  or 
penicillin  treatment,  but,  if  these  be  excepted,  and  they  are 
the  minority,  I have  never  yet  seen  reason  to  regard  the 
septic  fevers  more  anxiously  than,  for  instance,  the  typhoid 
group  of  fevers.  A reasonably  optimistic  prognosis,  which 
recognizes  the  natural  tendency  of  otherwise  healthy  patients 
to  recover  from  their  acute  bacterial  illnesses,  has  a real 
practical  value  and  may  considerably  influence  the  handling 
of  cases.  Prognosis  depends  more  for  its  accuracy  on  a know- 
ledge of  the  natural  history  of  a disease  than  on  any  other 
circumstance.  The  present  small  series  only  supports  my 
experience  of  other  cases  of  staphylococcal  fever  seen  during 
the  war  of  1014-18  and  in  hospital.  Given  asound  physique, 
a reasonably  early  diagnosis,  a good  Icucocytosis,  and  watch- 
ful care,  the  majority  of  cases  should  recover,  although  the 
course  of  the  disease  is  often  very  prolonged.  In  this  scries, 
after  excluding  those  of  lesser  severity  and  labelled  as  bac- 
teriaemia — cases  which  determined  their  favourable  course 
and  recovery  by  forming  a spontaneous  fixation  abscess — wc 
are  left  with  five  gravely  septicaemic  cases,  and  one  case 
of  serious  renal  infection.  Of  the  five  septicaemic  cases 
one  died.  The  remainder  made  complete  recoveries  with 
the  exception  of  Case  4,  in  which  local  disability  from  the 
damaged  femur  is  likely  to  persist.  In  the  fatal  case  the 
adverse  features  from  the  beginning  were  an  unhealthy  type 
of  physique,  notoriously  non-resistent  to  infection,  and  a 
poor  leucocytic  response.  In  addition,  surgical  treatment  of 
the  primary  focus  was  delayed  and  an  important  secondary 
renal  focus  was  not  touched.  Finally,  the  accident  of  a 
cerebral  metastasis  determined  death  at  a time  when  there 
had  been  definite  clinical  improvements  in  respect  of  general 


TREATMENT  OF  STAPHYLOCOCCAL  FEVER  229 
physical  and  mental  symptoms.  It  might  be  aTgued  that 
the  remaining  four  cases  were  not  representatively  severe. 
As  a matter  of  fact  and  in  terms  of  hospital  classification,  all 
would  have  found  a place  on  the  ‘danger  list’  over  periods 
of  many  weeks.  Multiple  cardiac  and  cerebral  metastases 
are  probably  always  fatal,  but  pulmonary  abscesses,  even 
in  great  numbers,  are  consistent  with  perfect  recovery,  and 
without  surgical  interference  as  they  are  spontaneously 
evacuated. 

Treatment.  If  an  appreciation  of  the  natural  history  of  a 
disease  is  important  for  prognosis  it  is  equally  or  more  so  for 
treatment.  A further  reference  to  the  methods  and  opinions 
of  Sir  William  Gull  may  here  be  deemed  appropriate.  At  a 
time  when  various  remedies  for  rheumatic  fever  were  being 
vaunted,  Gull  decided  that  without  a knowledge  of  the 
natural  course  of  the  untreated  disease  it  was  impossible  to 
judge  the  efficacy  of  therapeutic  measures.  He  therefore 
reported  with  close  care  and  the  collaboration  of  Dr.  H.  G. 
Sutton  a series  of  cases  treated,  apart  from  nursing  and  symp- 
tomatic measures,  by  mint  water  alone.1  His  conclusions 
were  to  the  effect  that  there  was  no  evidence  that  the  course 
of  the  disease  was  influenced  by  the  supposedly  specific 
remedies.  The  work  was  a model  of  reasoned  clinical  research. 
It  is  to  be  wished  that  judicial  inquiries  of  this  kind  were 
more  prevalent  to-day.  For  over  twenty  years  in  septic 
states  sera,  vaccines  and  non-specific  chemotherapy  were  in 
fashion,  but  it  must  be  confessed  that  their  prescription 
commonly  had  as  slender  a basis  in  reason  and  systematic 
controls  as  had  the  old  rheumatic  remedies.  Their  advocacy 
could  be  traced  largely  to  the  laboratory  specialists,  whose 
training  and  primary  interest  were  in  respect  of  the  agents 
of  disease,  whose  contacts  with  patients  were  small,  and  who 
had  in  consequence  but  a nodding  acquaintance  with  the 
natural  history  of  disease.  Whatever  virtue  vaccines  may 
have  in  the  case  of  local  infection  I have  never  been  able  to 
understand  their  rationale  in  a generalized  infection.  When 

1 ‘Cases  of  Rheumatic  Fever,  treated  for  the  most  part  by  Jlint  Water*, 
anil  ‘Remarks  on  the  Natural  History  of  Rheumatic  Fever',  A Collection  of 
the  Published  Writings  of  Sir  William  Gull,  New  Sydenham  Society,  1804. 


230  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
the  body  is  competing  with  a vast  invasion  of  living  organ- 
isms, it  can  scarcely  be  regarded  as  a sound  principle  to 
inoculate  it  with  a few  more  millions  of  dead  organisms;  in 
practice  I have  never  yet  been  assured  of  resultant  benefits. 
Nor  have  I seen  good  done  by  injections  of  eusol  or  mercuro- 
chrome  in  cases  of  septicaemia,  or  been  persuaded  by  the 
literature  of  the  subject  that  the  happy  results  which  some- 
times followed  the  treatment  were  due  to  it.  Again,  on  the 
score  of  reason,  it  seems  at  least  unlikely  that  a small  amount 
of  antiseptic,  further  diluted  in  many  pints  of  circulating 
blood,  will  materially  influence  a thriving  blood-stream  in- 
fection. A successful  chemotherapy  for  bacterial  disease,  it  is 
now  shown,  must  be  based  on  other  principles  than  simple 
antisepsis.  There  is  one  further  objection  to  the  use  of 
pseudo-specific  therapies,  and  that  is  that  they  are  apt  to 
impart,  at  a time  of  necessary  anxiety,  a sense  of  security,  a 
feeling  that  ‘something  is  being  done’,  thereby  leading  at 
times  to  a neglect  of  elementary,  but  none  the  less  important 
and  better  proven,  measures  of  treatment.  Of  his  own  expec- 
tant, observant  method  Gull  truly  remarked,  ‘It  required 
often  more  consideration  than  was  requisite  for  prescribing 
any  supposed  appropriate  drug  treatment.  ’ Sulphonamides 
were  only  a little  more  encouraging  than  other  chemical 
treatment  in  the  staphylococcal  fevers,  but  penicillin  has 
now  established  its  benefit  beyond  dispute. 

The  general  principles  of  non-specific  treatment  in  staphy- 
lococcal fever  may  be  briefly  summarized  under  three  head- 
ings: (1)  good  nursing,  (2)  a copious  fluid  intake  of  at  least 
six  pints  of  fluid  in  the  twenty-four  hours  for  an  adult,  and 
(3)  watchful  clinical  care  for  metastatic  abscesses  and  con- 
sidered judgement  which  to  open  and  when  to  open  them. 
Osteomyelitis  once  called  for  early  operation,  but  penicillin 
has  made  drastic  and  early  intervention  less  necessary.  An 
established  perinephric  abscess  should  be  dealt  with  without 
delay.  The  loin  may  sometimes  be  incised  with  advantage 
in  perinephritis  even  though  no  pus  be  found.  Abscesses  in 
skin  and  muscle  should  be  opened  when  ‘ ripe’.  The  pulmo- 
nary abscesses  are  better  left  to  themselves.  Pleuritic  fluid 
may  be  aspirated.  Should  a stage  of  weakness  and  low 


TREATMENT  OF  STAPHYLOCOCCAL  FEVER  231 
fever  without  organisms  in  the  blood-stream  follow  upon  an 
acute  septieaemic  phase,  sunshine  and  fresh  air  are  invaluable 
adjuncts  to  treatment.  Even  a slight  persistent  pyrexia 
should,  however,  suggest  the  possibility  of  a hidden  abscess 
and  the  body  should  be  searched  systematically  with  a finger- 
tip in  likely  regions  for  any  tender  point  or  points.  If  there 
is  any  suspicion  of  a focus  in  bone,  a careful  radiological 
examination  is  also  necessary.  Sir  Charles  Symonds  once 
described  to  me  a case  of  staphylococcal  septicaemia  compli- 
cated by  cervical  root  pains  and  some  dysphagia.  Later, 
when  the  septicaemia  had  subsided,  convalescence  was 
retarded  by  continued  low  fever.  Eventually  a second  set 
of  radiograms  of  the  neck  was  taken,  revealing  extensive 
destruction  of  the  fourth  cervical  vertebra  by  osteomyelitis, 
in  spite  of  which  the  patient  had  retained  free  movements 
of  the  head  and  neck. 


Summary 

Staphylococcal  infections  of  the  skin  are  complicated 
from  time  to  time  by  a blood-stream  invasion.  This  may 
take  a benign  form  (bacteriacmia)  and  produce  a single 
‘fixation  ’ metastasis,  or  several  small  abscesses  without  real 
danger  to  life.  Alternatively  there  may  result  a severe 
form  (septicaemia  or  pyaemia)  with  prolonged  fever,  rigors, 
sweats,  multiple  metastases,  and  positive  blood  cultures. 
The  favourite  site  of  localization  in  adult  life  is  the  renal 
cortex,  usually  with  secondary  perinephritis  or  perinephric 
abscess.  Other  tissues  frequently  involved  are  the  lungs,  the 
skin,  the  muscles,  and  the  prostate  gland.  Brain  abscess  is  a 
rare  and  grave  complication.  The  differential  diagnosis  from 
streptococcal  fever  is  made  by  the  tendency  to  the  develop- 
ment of  multiple  abscesses  in  the  tissues  named ; the  absence, 
as  a rule,  of  infection  in  joint  cavities  and  other  cavities  lined 
by  serous  membranes  (excepting  when  infection  spreads 
from  the  lung  to  the  pleura  or  from  bone  to  joint);  the 
absence  of  glossitis,  diarrhoea,  and  progressive  anaemia; 
the  relatively  slow  pulse ; and  by  blood  culture. 

Lung-complications  with  haemoptyses  and  profuse  sweats 
may  lead  to  a faulty  diagnosis  of  pulmonary  tuberculosis. 


232  NATURAL  HISTORY  OF  STAFI1YLOCOCCAL  FEVER 
Perinephritis  or  a vertebral  metastasis  may  lead  to  a dia- 
gnosis of  spinal  or  hip  disease.  Prolonged  initial  fever  with- 
out obvious  metastascs  may  lead  to  a diagnosis  of  typhoid 
fever,  but  the  sweats,  the  rarity  of  splenic  enlargement,  the 
absence  of  rose-spots,  the  leucocyte  count,  and  a blood 
culture  help  to  establish  the  correct  opinion.  In  both  diseases 
the  pulse  tends  to  remain  slow  at  first.  In  every  case  of 
obscure  continued  fever  a careful  inquiry  should  be  made 
in  regard  to  recent  carbuncle  or  furunculosis,  or,  in  fact,  to 
any  history  of  local  skin  infection  at  any  time  in  the  previous 
three  to  six  months.  With  youth  and  a good  Icucocytosis  the 
prognosis  in  staphylococcal  septicaemia  is  by  no  means  bad. 
With  penicillin,  watchful  care,  good  nursing,  a copious  fluid 
intake,  surgical  treatment  of  abscesses  which  can  be  readily 
approached,  and  sunshine  and  fresh  air  in  convalescence, 
there  is  a good  prospect  of  complete  recovery.  The  early 
appearance  of  a natural  fixation  abscess  is  a favourable 
feature.  Vaccine  therapy  should  be  avoided  at  all  stages. 
Drastic  surgical  intervention  has  now  become  much  less 
necessary,  even  in  cases  with  bone  infection. 


XVII 

THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
TREATMENT  OF  STREPTOCOCCAL  FEVER 

In  the  previous  lecture  an  attempt  was  made  to  portray 
the  essential  clinical  features  of  generalized  and  metastatic 
infections  with  Staphylococcus  aureus.  It  was  shown  that 
the  primary  focus  was  usually  to  be  found  in  a boil  or  other 
superficial  skin  lesion  and  that,  although  the  sequels  of  a 
blood-stream  invasion  were  very  varied,  certain  sympto- 
matic and  historical  peculiarities  made  it  convenient  to 
review  staphylococcal  bacteriaemia  and  septicaemia  (to- 
gether with  renal  carbuncle  and  osteomyelitis)  under  a 
single  heading,  regarding  them  collectively  as  the  manifes- 
tations of  a specific  fever. 

The  same  treatment  is  possible  in  the  case  of  streptococcal 
bacteriaemia  and  septicaemia,  but  here  we  are  confronted 
with  greater  difficulties  of  presentation  because  the  strains 
of  streptococcus  capable  of  causing  blood-poisoning  are 
many  and  the  possible  routes  of  invasion  numerous,  the 
natural  course  of  the  disease  being  much  influenced  by  these 
and  other  factors.  Scarlet  fever,  erysipelas,  puerperal  fever, 
and,  in  most  instances,  infective  endocarditis,  are  strepto- 
coccal fevers,  but  it  would  clearly  be  unsound  to  confine 
them  within  a single  category.  The  natural  history  of  the 
diseases  named  and  the  bacterial  strains  involved  separate 
them  from  each  other  far  more  widely,  for  instance,  than 
the  individual  members  of  the  typhoid  group  are  separable. 
Furthermore,  scarlet  fever  and  erysipelas  may  themselves 
be  complicated  by  a streptococcal  septicaemia  clinically 
comparable  with  the  * surgical’  and  ‘ obstetric’  septicaemias, 
and  yet  not  to  be  considered  as  an  essential  part  of  the 
primary  disease.  Epidemic  influenza  may  also  be  com- 
plicated by  a streptococcal  septicaemia,  and  the  merging 
of  the  two  diseases  creates  a clinical  picture  unlike  that 
produced  by  either  disease  alone.  A terminal  streptococcal 


231  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
septicaemia  is  not  rare  in  severe  debilitating'  diseases,  and 
particularly  in  those  marked  by  a grave  anaemia;  here  the 
septicaemia  is  merely  an  incident  due  to  an  invasion  of 
tissues  deprived  of  their  proper  nutriment  and  resisting 
powers. 

These  difficulties  notwithstanding,  it  is  possible  to  select 
cases  illustrating  types  of  streptococcal  fever  sufficiently 
distinct  in  their  clinical  behaviour  and  pathology  to  warrant 
separate  consideration.  Whether  from  the  point  of  view  of 
diagnosis,  prognosis,  or  treatment,  such  separate  considera- 
tion is  useful.  Once  more,  as  with  the  staphylococcal  cases, 
we  may  draw  a useful  distinction  between  streptococcal 
bacterincmia  and  septicaemia.  The  term  streptococcal  fever 
is  intended  to  include  both.  It  is  employed  partly  to  foster 
the  analogy  of  a specific  bacterial  disease  or  a group  of 
specific  bacterial  diseases,  and  partly  to  avoid  a certain 
ambiguity  which  attaches  to  the  word  septicaemia.  Do  we 
in  using  it  distinguish  sufficiently  between  a condition  in 
which  organisms  arc  finding  their  way  into  the  blood -stream 
and  may  occasionally  or  momentarily  be  demonstrable  there, 
and  one  in  which  they  are  actively  thriving  and  multiplying 
in  the  body  fluids  ? The  anxiety  engendered  by  a laboratory 
diagnosis  of  septicaemia  becomes  greatly  mitigated  when 
clinical  judgement  can  insist  that  a particular  case  exem- 
plifies the  former  rather  than  the  latter  event.  On  the  other 
hand,  can  we  always  exclude  as  non-scpticaemic  cases 
which  have  all  the  clinical  characters  of  a septicaemia,  but 
which  give  negative  cultural  results?  On  the  analogy  of 
typhoid  fever  and  infective  endocarditis  we  cannot  do  so, 
for  in  these  diseases  there  is  a considerable  percentage  of 
cases  in  which  blood  cultures  remain  sterile.  For  the  dia- 
gnosis of  bacteriacmia  and  septicaemia  wc  must  ever 
require  a proper  balancing  of  all  the  available  evidence 
whether  obtained  at  the  bedside  or  in  the  laboratory. 

In  this  paper  it  is  proposed  to  consider  with  illustrations 
(a)  the  aetiology  and  paths  of  invasion ; (6)  the  outstanding 
clinical  features  and  differential  diagnosis ; (c)  the  prognosis ; 
and  (d)  the  treatment  of  streptococcal  fevers  other  than 
scarlet  fever,  erysipelas,  and  infective  endocarditis. 


TREATMENT  OF  STREPTOCOCCAL  FEVER 


235 


(a)  Aetiology  and  Paths  of  Invasion 

Age  and  sex  would  seem  to  have  little  or  no  influence  on 
the  incidence  of  streptococcal  fever  if  we  exclude  the  puer- 
peral cases.  Season  has  its  influence  only  in  so  far  as  it  helps 
to  determine  epidemics  of  influenza  or  of  the  exanthemata 
or  throat  infections  commonly  complicated  by  sinus  in- 
flammation and  middle-ear  disease.  Fatigue  may  play  a 
part,  and  it  is  commonly  held  that  the  overworked  surgeon 
in  need  of  a holiday  is  more  liable  to  fall  a victim  to  grave 
sepsis  than  one  in  happier  circumstances.  Exhaustion  such 
as  obtains  after  a difficult  labour  may  be  reasonably  re- 
garded as  a factor  in  puerperal  fever,  although  it  can 
scarcely  be  said  to  operate  except  in  concert  with  other 
factors  such  as  anaemia  and  local  trauma.  If  surgical 
injuries  be  excluded,  the  most  apparent  causes  predisposing 
to  streptococcal  fever  are  (1)  other  infections,  and  (2) 
anaemia.  Influenza,  scarlet  fever,  measles,  and  staphylo- 
coccal infections,  whether  local  or  general,  may  all  pave  the 
way  for  a streptococcal  invasion.  Grave  anaemias,  as  has 
been  mentioned,  may  terminate  fatally  with  a streptococcal 
septicaemia  which  is  usually  brief  in  its  course  and  masked 
by  the  symptoms  of  the  antecedent  disease. 

While  staphylococcal  fever  originates  in  some  surface 
lesion  of  the  skin  such  as  a boil  or  carbuncle,  streptococcal 
fever  may  date  its  inception  from  an  invasion  of  a cutaneous 
or  a mucous  surface  or  deeper  structures,  and  may  occur 
without  an  evident  local  focus.  Wounds  so  trivial  as  a needle- 
prick  or  a hang-nail  may  provide  the  portal  of  entry  for  a 
virulent  infection  and  determine  a septicaemia  as  devastat- 
ing in  its  consequences  as  one  acquired  through  a severe  war- 
wound  or  the  placental  site.  The  following  list,  without  pre- 
tensions to  completeness,  indicates  the  vide  variety  of  causes, 
sites,  or  modes  of  infection  which  may  be  encountered: 
(I)  a needle-prick  or  hang-nail,  particularly  in  the  case  of 
surgeons,  nurses,  and  morbid  anatomists ; (2)  any  punctured 
wound  or  laceration;  (3)  a com  infected  by  injudicious 
paring;  (4)  a mosquito-bite;  (5)  an  infected  haematoma; 
(6)  a tonsillitis ; (7)  a throat  infection  in  patients  from  whom 


230  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
the  tonsils  have  been  removed  and  sometimes  in  that  event 
with  little  or  no  local  soreness  or  redness;  (8)  a middle-ear 
infection  with,  or  more  rarely  without,  evident  mastoiditis 
or  lateral  sinus  thrombosis ; (9)  infection  of  one  or  more  of 
the  accessory  sinuses;  (10)  an  infected  tooth  socket,  without 
or  following  extraction;  (11)  the  uterus  after  a confinement 
or  abortion ; (12)  an  acutely  inflamed  viscus  with  peritoneal 
infection.  A skin  infection  may  lead  first  to  a whitlow  or  to 
a local  or  spreading  cellulitis,  to  a lymphangitis,  or  to  a sup- 
purative adenitis,  or  alternatively  without  any  contiguous 
spread  or  evidence  of  active  co-operation  on  the  part  of 
the  natural  lymphatic  barriers,  a small  red  spot  or  local 
lymphangitis  is  succeeded  by  a rigor  and  a rapidly  develop- 
ing septicaemia.  Given  a virulent  infection  the  less  the 
lymphatic  defences  are  called  into  play  the  greater,  of 
course,  is  the  likelihood  of  a grave  general  infection.  In  some 
fulminating  infections,  whether  originating  in  a cutaneous 
wound  or  a throat  infection  or  elsewhere,  it  would  thus 
seem  that  the  organisms  pass  directly  into  the  circulation 
and  that  the  lymphatic  system  has  been  ‘caught  napping’. 
In  the  particular  case  of  the  surgeon  and  the  pathologist 
we  may  sensibly  argue  that  the  virulence  has  been  recently 
increased  by  ‘passage*. 

(6)  Outstanding  Clinical  Featuees 
Rigor  or  high  fever  with  chilliness  and  malaise  is  the  first 
manifestation  of  streptococcal  fever.  Repeated  rigors  are 
perhaps  more  frequent  in  streptococcal  than  in  staphylo- 
coccal fever,  and  this  may  be  correlated  with  a lesser  ten- 
dency to  the  formation  of  spontaneous  fixation  abscesses  in 
the  former.  In  the  graver  cases  the  temperature  rapidly  soars 
to  101°  or  103°  or  even  higher,  and  death  may  ensue  within 
a few  days  or  even  within  twenty-four  hours.  In  cases  which 
survive  the  initial  onslaught  the  temperature  maintains 
a general  high  level  at  first  with  considerable  diurnal 
oscillations.  In  the  more  chronic  cases  and  stages  there  is 
a regularly  remittent  or  intermittent  pyrexial  curve  such  as 
is  also  seen  in  streptococcal  infective  endocarditis.  Charts 
A and  B (pp.  241,  242)  illustrate  the  first  three  weeks  and  a 


TREATMENT  OF  STREPTOCOCCAL  FEVER  237 
period  of  three  weeks  shortly  before  the  final  defervescence  in 
a severe  case  of  septicaemia  due  to  a haemolytic  streptococcus 
(Case  2).  The  total  period  of  fever  was  here  about  twelve 
weeks.  With  the  stage  of  high  fever  go  delirium,  prostra- 
tion, restlessness,  sighing,  vomiting,  a dry,  red  tongue,  and 
splenic  enlargement.  The  spleen  may  enlarge  very  rapidly 
and  considerably,  but  at  first  it  is  so  soft  as  not  to  be  readily 
palpated.  This  is  explained  by  the  fact  that  in  fatal  cases 
the  spleen  pulp  at  necropsy  is  found  to  be  almost  diffluent. 
High  fever,  rigor,  delirium,  and  prostration  can  proclaim 
any  septicaemia,  but  there  are  four  manifestations  which 
may  be  regarded  as  peculiarly  diagnostic  of  streptococcal 
fever  and  as  expressing,  I believe,  infection  with  a haemo- 
lytic strain.  These  are:  (1)  diarrhoea,  often  frequent  and 
troublesome;  (2)  the  presence  of  albuminuria  with  red 
cells  and  casts  in  the  urinary  deposit  and  occasionally  a 
smoky  urine;  (3)  rapidly  progressive  anaemia;  and  (4)  a 
smooth,  red,  desquamated,  and  sore  tongue.  Some  or  all 
of  these  findings  are  common  in  puerperal  septicaemia, 
which  is  so  often  due  to  a haemolytic  strain,  but  I have 
seen  them  just  as  manifest  in  other  cases,  and  first  became 
familiar  with  them  while  in  charge  of  chest-wounds  during 
the  1914-18  War  The  diarrhoea  of  puerperal  septicaemia  is 
commonly  attributed  to  the  local  peritonitis,  but  as  it 
occurs  also  in  non-peritonitic  cases,  this  requires  qualifica- 
tion. A representative  case  under  the  care  of  Sir  Arthur 
Hurst,  previously  reported  by  me  in  the  Clinical  Journal, 
April  1922,  may  be  requoted  here. 

Case  1 . Charlotte I.,  aged  23,  and  married,  was  admitted  for  pains 
in  the  right  buttock  and  diarrhoea  on  20  February  1920.  Five  weeks 
previously  she  had  had  an  attack  of  * tonsillitis  and  influenza’.  Three 
weeks  later  she  had  a double  quinsy,  which  was  opened.  On  22  Feb- 
ruary she  developed  uncontrollable  diarrhoea  and  vomiting.  The  next 
day  symptoms  persisted  and  she  had  sharp  pain  in  the  right  buttock 
and  pain  on  moving  the  right  leg.  On  admission  her  temperature  was 
104°,  pulse  122,  respiration-rate  20 ; cheeks  flushed ; tonsils  large  and 
red;  the  spleen  just  palpable.  The  urine  contained  albumin,  red  cells, 
leucocytes,  and  granular  casts.  Leucocyte  count  12,000  cells  per  cub. 
mm.  on  27  February.  There  was  tenderness  over  the  sacro- iliac  joint. 
Cultivations  from  the  urine  were  sterile.  From  the  faeces  B.  coli 
and  Streptococcus  longus  were  grown;  from  the  throat  Micrococcus 


233  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
catanhalis,  Staphylococci,  and  Streptococcus  longus.  On  7 March  blood 
cultivations  grew  Streptococcus  longus.  Between  12  and  18  March 
120  c.c.  of  polyvnlcnt  anti-strcptococcus  serum  were  given  intra- 
venously, and  two  rigors  were  recorded.  On  20  March,  although  the 
temperature  at  the  time  was  101°,  blood  cultivations  were  negative. 
On  31  March  albumin  having  disappeared  from  the  urine  some  days 
previously,  both  legs  suddenly  became  oedematous  without  signs  of 
venous  thrombosis.  The  oedema  soon  subsided,  the  temperature  fell 
by  lysis,  and  the  patient  was  discharged  well  on  9 May.  No  local 
developments  calling  for  surgical  intervention  were  recorded.  The 
serum,  which  was  administered  late,  as  the  infecting  organism  was 
not  at  first  determined,  produced  no  striking  effect  on  the  pyrexlal 
curve. 

The  special  manifestations  described  above  are  perhaps 
an  index  of  the  highly  cytolytic  properties  of  the  bacterial 
toxins  elaborated  by  haemolytic  strains.  It  is  reasonable  to 
suppose  that  both  the  nephritis  and  the  cntero-colitis  are 
due  to  a toxic  rather  than  a local  bacterial  action,  sustained 
by  the  kidneys  and  bowel  in  their  attempt  to  excrete  these 
poisons.  In  favour  of  this  supposition  I can  quote  a ease  of 
streptococcal  fever  in  which  these  special  symptoms  were 
present,  resulting  from  a local  pelvic  peritonitis  uritltout 
septicaemia,  with  a negative  blood  culture,  and  showing 
rapid  recovery  after  local  surgical  drainage. 

The  pulse-rate  in  streptococcal  fever  is  rapid  from  the 
beginning,  when  figures  of  120  and  upwards  arc  commonly 
recorded.  In  the  nbsence  of  lung  complications  the  respira- 
tory rate  is  not  considerably  raised,  a useful  distinction 
from  the  pneumococcal  fevers.  Various  rashes — scarlatini- 
form,  morbilliform,  or  a blotchy  erythema,  and  more  rarely 
petechial  haemorrhages— may  appear  within  the  first  few 
days,  and  are  usually  transitory.  Icterus  may  complicate 
the  haemolytic  infections.  Venous  thromboses  occur  as  in 
other  septicaemias.  In  cases  which  survive  the  first  few 
days  there  is  generally  a leucocytosis  varying  from  12,000 
to  30,000  cells  per  cub.  mm.  The  haemoglobin  in  the 
haemolytic  infections  falls  rapidly  to  figures  as  low  as  20 
or  30  per  cent.  Apart  from  haemorrhage  and  the  acute 
leukaemias  there  are  probably  no  diseases  in  which  a severe 
secondary  anaemia  develops  so  abruptly.  The  diarrhoea 
is  not  as  a rule  accompanied  by  the  passage  of  blood  and 


TREATMENT  OF  STREPTOCOCCAL  FEVER  239 
mucus.  The  nephritis  is  usually  transient  and  not  accom- 
panied by  signs  of  renal  inadequacy.  Emaciation  takes 
place  with  great  rapidity  in  the  graver  cases.  A lobar 
pneumonia  may  also  complicate  a streptococcal  invasion. 
When  such  a pneumonia  is  accompanied  by  anaemia  and 
is  slow  to  resolve,  lung  puncture  will  probably  give  a haemo- 
lytic streptococcus.  Although  delirium  has  been  mentioned 
as  an  early  symptom,  there  may  be  a quite  remarkable 
mental  acuity.  Trousseau  gives  a vivid  description  of  this 
in  his  account  of  the  puerperal  cases,  contrasting  it  with 
the  grievous  physical  plight  of  the  poor  victims.  He  also 
lays  emphasis  on  diarrhoea  as  a leading  symptom. 

A streptococcal  septicaemia  may  run  its  course  to  death 
or  recovery  with  or  without  metastatic  symptoms.  The 
favourite  localizations  are  in  cavities  lined  by  serous  mem- 
branes. The  medium  or  larger  joints,  the  pleural  sacs,  the 
pericardium,  the  meninges,  and  the  peritoneum  are  affected 
probably  in  this  order  of  frequency.  R.  E.  Smith*  has  drawn 
particular  attention  to  the  close  simulation  of  a true  in- 
fective arthritis  by  peri-articular  inflammations  in  the  cel- 
lular planes. 

The  clinical  diagnosis  of  streptococcal  fever  (septicaemia 
type)  may,  in  brief,  be  based  upon  the  association  of  high 
fever,  rigor,  quick  pulse,  delirium  or  an  over-alert  mentality, 
rapid  splenic  enlargement  and  metastatic  infection  of  serous 
cavities.  To  these  may  be  added  diarrhoea,  sore  tongue, 
nephritis,  and  anaemia  in  some  cases  of  infection  with 
haemolytic  strains.  A careful  inquiry  with  regard  to  pos- 
sible sites  of  invasion  is  clearly  of  the  first  importance. 

The  differential  diagnosis  from  staphylococcal  fever  has 
been  described  in  some  detail  in  the  previous  lecture. 
Suffice  it  to  say  that  in  staphylococcal  fever  a history  of 
boils  or  a carbuncle,  a slow  initial  pulse-rate,  the  liability 
to  the  formation  of  abscesses  in  the  renal  cortex  and  to 
osteomyelitis  are  characteristic,  and  that  splenic  enlarge- 
ment and  involvement  of  serous  cavities  are  rare.  Pneu- 
mococcal fever  may  also  present  difficulties.  The  absence 
of  any  primary  focus;  the  hot,  dry  skin;  herpes  labialis; 

1 Gun's  Hasp.  Reports,  1931,  Uxxi.  1. 


240  TIIE  NATURAL  HISTORY,  PROGNOSIS,  AND 
and  the  considerable  rise  in  the  respiration  rote  even  in  the 
absence  of  patent  lung  signs  arc  among  the  distinguishing 
features,  but  the  pneumococcus,  although  favouring  lung, 
pleura,  and  pericardium,  may  also  settle  in  joints  and  the 
meninges  and,  in  peritonitic  cases  especially,  can  cause 
diarrhoea. 

As  always,  it  is  the  cases  or  stages  with  fever  alone  and 
lacking  local  manifestations  that  present  the  greatest  diffi- 
culties. Here  the  leucocyte  count  to  exclude  a typhoid 
group  infection  and  blood  cultivation,  which  should  ideally 
be  made  in  every  ease  of  obscure  and  anxious  fever,  will 
have  their  special  value. 

In  streptococcal  fever  (bacteriaemic  type)  the  constitu- 
tional disturbance  is  less  severe,  the  pulse-rate  less  soaring, 
repeated  rigors  are  not  observed,  and  exhaustion  and 
anaemia  are  less  evident,  but  metastatic  infections  may 
equally  well  occur  ( vide  Case  C).  Alternatively,  the  fever 
may  be  traced  to  a localized  infection,  as  in  the  case  of 
pelvic  peritonitis  referred  to  above. 

In  the  case-histories  reported  hereunder  the  varying 
modes  of  origin  and  the  diverse  complications  find  free 
illustration,  but  it  may  be  claimed  that  a sufficient  similarity 
in  clinical  course  and  history  becomes  apparent  in  their 
perusal  to  warrant  the  inclusion  of  all  the  cases  under  the 
single  heading  of  Streptococcal  Fever. 

Cash  2.  Streptococcal  Fever  (Septicaemia)  following  a Staphylococcal 
Infection.  Multiple  Arthritis.  Recovery.  A young  married  woman, 
shortly  after  o confinement,  developed  a furuncle  in  the  meatus  of  her 
left  ear.  This  was  complicated  by  a suppurative  parotitis  on  the  same 
side,  the  infecting  organism  being  reported  as  Staphylococcus  aureus. 
Three  weeks  later,  when  apparently  almost  convalescent  from  this 
but  still  troubled  with  a salivary  fistula  and  slight  pyrexia,  she  became 
suddenly  ill  and  developed  a diffuse  rash,  at  first  morbilliform,  then 
scarlat  ini  form,  and,  when  I first  saw  her,  appearing  os  a diffuse  ery- 
thema. The  temperature  rose  .to  105°;  pulse  140;  respirations  £8. 
The  spleen  was  palpable  and  tender.  Blood  cultures  grew  profuse 
colonies  of  a haemolytic  streptococcus  witliin  twelve  hours.  Leuco- 
cyte count  2 4,000  cells  per  c nun.  On  the  next  day  she  was  worse, 
with  irregular  breathing  and  apnoeic  pauses,  and  vomiting  was 
frequent.  On  the  second  day  of  the  illness  she  was  given  40  c.c. 
of  mixed  polyvalent  anti-streptococcus  serum  subcutaneously.  On 


TREATMENT  OF  STREPTOCOCCAL  FEVER  241 
each  of  the  three  following  days  she  was  given  60  c.c.  of  mixed  scrum 
(i.e.  from  several  big  manufacturing  firms)  intravenously,  -without 
apparent  benefit.  Rigors  occurred  at  intervals  during  the  first  -week 
(vide  Chart  A).  On  the  fifth  day  effusion  occurred  into  a knee-joint, 
and  was  aspirated  then  and  on  the  seventh  day.  At  a later  date  the 
joint  was  drained.  Other  joints  became  inflamed  and  swollen,  but 
Inter  subsided.  Liberal  fluids,  glucose,  and  alkalis  were  given  by 


Chart  A.  Initial  phase. 


mouth,  and  glucose  with  saline  per  rectum.  Omnopon  was  given  at 
night  for  pain.  The  total  duration  of  the  fever  was  twelve  weeks. 
Latterly  emaciation  was  very  marked,  and  there  was  a continued 
low-grade  pyrexia.  At  this  stage  she  was  seen  by  Lord  Horder,  who 
discovered  a tender  point  in  the  muscles  above  the  infected  knee. 
A small  abscess  here  was  drained,  and  thereafter  the  temperature 
soon  returned  to  normal  and  convalescence  was  not  seriously  inter- 
rupted. With  the  exception  of  a partially  stiff  knee,  recovery  was 
complete.  Expert  and  devoted  nursing,  a copious  fluid  intake  {even 
at  the  height  of  her  illness  this  patient  took  from  six  to  eight  pints  of 
milk  in  the  day  as  well  as  other  fluids),  and  timely  surgery  impressed 
me  as  the  most  serviceable  elements  in  the  treatment. 

Case  3.  Streptococcal  Fever  ( Septicaemia ) complicating  Influenza. 
Frontal  Sinus  Infection.  Hyperpyrexia.  Death.  A male  worker  in  a 
n 


242  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
sweet  factory,  where  he  had  been  working  overtime,  developed  a 
cold  on  8 December  1025.  During  the  next  two  days  his  letters  home 
were  reported  as  ‘strange*.  On  10  December  he  was  seen  by  Dr.  A.  II. 
Elliott,  with  headache,  generalized  pains,  and  a temperature  of  102®. 
A blotchy  rash  was  also  noted  in  the  groins  and  extending  down  the 
legs.  On  12  December  I was  asked  to  sec  him.  He  was  delirious, 
truculent,  and  would  not  stay  in  bed,  which,  he  declared,  was  occupied 


Cjlabt  B.  Phase  preceding  final  defervescence. 


by  someone  else.  It  was  very  difficult  to  examine  him.  His  tongue 
was  coated  with  a yellowish  fur ; throat  very  red,  with  a film  of  muco- 
purulent exudate;  slight  oedema  around  left  orbit;  pulse  120;  rapid 
breathing,  but  no  distress ; his  feet  had  a curious  purplish  colour  when 
he  sat  up ; the  spleen  was  not  palpable ; and  there  were  no  pneumonic 
signs.  He  was  sent  into  hospital,  and  was  very  violent  on  arrival. 
His  temperature  rose  to  10S®  in  the  axilla  and  he  died  the  same  night. 
I diagnosed  Inffuenzo-strcptoeoccal  septicaemia,  and  on  the  analog?' 
of  cases  recorded  in  the  1918-10  epidemic  suggested  that  pus  would 
be  found  in  the  sphenoidal  cells  at  autopsy.  This  was  the  only  tiling 
found,  with  the  exception  of  a large  soft  spleen  and  some  pus  in  the 
gall-bladder.  Blood  cultures  and  the  pus  both  grew  a non*haemolytie 
streptococcus.  Streptococcus  viridans  was  grown  from  the  cerebro- 
spinal fluid  and  the  heart’s  blood. 


243 


TREATMENT  OF  STREPTOCOCCAL  FESTER 

Case  4.  Streptococcal  Fever  (Septicaemia)  following  a Surgical 
Wound . Lymphangitis.  Cellulitis.  Spleen  Tumour.  Recovery.  A 
medical  man,  aged  28,  had  been  feeling  tired  and  out  of  sorts.  On 

9 October  1928  he  performed  an  operation  for  adenoids  on  a child 
whose  father  had  recently  had  a bad  tonsillitis.  He  barked  his 
knuckle  on  an  instrument.  By  the  next  morning  his  temperature 
was  103°,  he  felt  and  looked  very  ill,  and  bad  a line  of  lymphangitis 
spreading  up  the  arm.  There  were  no  enlarged  glands.  He  had  a pain 
in  the  left  lower  chest  and  was  very  restless  when  I saw  him  on  the 
evening  of  10  October.  His  pulse  varied  from  110  to  120.  He  was 
sweating  profusely.  I felt  very  anxious  about  him,  and  gave  him 

10  c.c.  of  scarlatinal  antitoxin  with  30  c.c.  of  polyvalent  antistrepto- 
coccic serum  intravenously.  Half  an  hour  later  he  had  a bad  rigor, 
and  then,  after  morphine,  passed  a good  night.  On  the  next  day  he 
was  distinctly  better,  with  pulse-rate  down  to  100.  I saw  him  again 
on  13  October.  The  temperature  had  risen  again  to  102°,  but  the 
general  condition  continued  to  improve ; much  swelling  of  dorsum  of 
hand;  lymphangitis  of  arm  less  evident;  still  complaining  of  discom- 
fort at  the  left  rib  maTgin,  especially  on  sitting  up.  I thought  I could 
feel  the  spleen.  I saw  him  again  on  20  October  with  Dr.  IV.  M. 
Etskine,  Dr.  H.  A.  Watney,  and  Mr.  E.  C.  Hughes,  his  improvement 
having  been  interrupted  by  further  pyrexial  spikes  and  some  fresh 
lymphangitis.  Except  in  the  pyrexial  attacks,  however,  his  pulse 
did  not  exceed  90  to  the  minute  and  appetite  was  good.  The  spleen 
was  now  large  and  firm,  and  extended  three  fingers  down  on  inspira- 
tion. The  history,  the  appearance  of  this  patient  on  the  first  day,  and 
the  subsequent  great  enlargement  of  the  spleen  {no  other  non-tropical 
fever  causes  such  rapid  enlargement)  were  eloquent  of  a streptococcal 
septicaemia.  The  general  impression  of  the  patient  and  his  medical 
advisers  was  that  the  septicaemia  had  terminated  after  the  adminis- 
tration of  the  serum,  and  that  the  subsequent  disturbances  were 
adequately  explained  by  the  local  sepsis.  The  case  was  seen  in  the 
country  and  facilities  for  blood  cultivation  were  not  to  hand.  Com- 
plete recovery  followed. 

Case  5.  Streptococcal  Fever  ( Septicaemia ) following  Difficult  Labour 
and  Manual  Removal  of  Placenta.  A woman  between  30  and  40  years 
of  age  was  confined  for  the  first  time.  She  had  previously  been 
anaemic  and  unfit.  There  was  an  instrumental  delivery  after  three 
days  of  pains,  and  the  placenta  was  removed  digitally.  That  evening 
she  had  a temperature  of  104°  and  a slight  rigor.  Four  days  later  she 
was  seen  by  an  obstetric  surgeon,  who  found  the  uterus  soft  and 
enlarged  up  to  the  navel,  feared  septicaemia,  and  put  a catheter  and 
glycerine  into  the  uterus.  Scarlatinal  antitoxin  (10  c.c.)  was  also 
given.  Diarrhoea,  which  had  been  troubling  her  slightly,  became 
profuse,  the  pulse-rate  rose  to  120,  and  1 was  asked  to  see  her  in 
consultation  on  the  fifth  or  sixth  day.  There  was  considerable 


214  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
abdominal  distension,  the  spleen  was  not  felt,  the  uterus  was  smaller. 
The  leucocyte  count  was  21,000 — a figure  which,  in  the  absence  of  an 
abscess  or  pneumonia,  suggests  septicaemia.  Haemoglobin  44  per 
cent.  The  diarrhoea  was  abating  and  there  was  slight  general  im- 
provement. A further  dose  of  antitoxin  was  given,  and  a few  days 
later  a Wood-transfusion.  Except  for  some  transient  signs  of  local 
peritonitis  in  the  right  lower  quadrant,  there  were  no  further  com- 
plications, and  recovery  followed. 

Case  6.  Streptococcal  Fever  (Bacteriaemia),  following  Tonsillitis 
and  Cellulitis  in  the  Neck.  Arthritis  of  Elbcrx.  Anaemia.  Ambulatory 
Case.  A man,  aged  61,  was  sent  to  see  me  on  14  March  1029.  One 
month  previously  he  had  had  a sore  throat,  and  then  one  day  at 
business  felt  very  chilly.  He  went  home,  nnd  was  there  treated  by 
Dr.  F.  J.  Aldridge  for  a brawny  swelling  in  the  right  side  of  the  neck 
which  made  swallowing  very  dill] cult,  ryrexia  lasted  only  n few  days, 
nnd  with  poultices  and  potassium  iodide  the  swelling  subsided. 
Thereafter  he  kept  about,  did  not  avail  himself  as  he  should  of  medical 
advice,  nnd  went  for  drives,  but  felt  ill  all  the  time.  Two  weeks  later 
he  developed  a swelling  on  the  inner  side  of  lus  left  ankle,  and  a week 
later  pain  and  swelling  in  the  left  elbow-joint.  Ilis  weight,  normally 
10  st.  0 lb.,  had  dropped  to  8 st.  10  lb.  He  was  pale  and  slightly 
dyspnoeic  with  the  effort  of  undressing.  His  pulse  was  very  rapid. 
There  was  one  septic  tooth  stump  in  the  upper  jaw  with  n cavity 
exuding  pus.  Haemoglobin  50  per  cent. ; leucocyte  count  10,650  per 
c.mm.  There  were  definite  signs  of  fluid  in  the  left  elbow-joint,  which 
was  tender  and  resistant  to  free  movement.  There  was  a painless, 
fluctuating  swelling  below  the  left  internal  malleolus.  Infection 
started  in  the  throat.  Anaemia  and  joint  infection  (unless  as  a com- 
plication of  neighbouring  osteomyelitis)  are  rare  in  staphylococcal 
bactcriacmin.  I therefore  suggested  a diagnosis  of  streptococcal 
bncteriaemia  with  metastatic  joint  infection  and  advised  admission  to 
hospital.  The  subsequent  lustory  of  this  case  has  not  been  obtained. 

Case  7.  Streptococcal  Fever  ( Septicaemia ) complicating  an  Osteo- 
myelitis of  Tibia.  Empyema.  Recovery.  Jn  the  latter  hall  of  3Iareb 
1029  a young  man,  aged  18,  developed  an  inflamed  area  over  his  right 
shin.  This  was  incised  as  a cellulitis.  Although  he  felt  well  in  himself 
and  was  afebrile,  the  wound  was  unsatisfactory  and  was  twice  re- 
opened. On  7 April  his  temperature  rose  suddenly  to  103°  and  he 
had  a rigor.  Thereafter  his  temperature  remained  high  and  he  pre- 
sented all  the  appearances  of  a septicaemia.  Cultures  from  the  wound, 
which  was  being  treated  with  eusol,  remained  sterile,  but  a strepto- 
coccus was  grown  from  the  blood.  Radiograms  of  the  leg  showed  a 
central  necrotic  area  in  the  tibia.  Mr.  L.  Bromley  operated,  removing 
necrotic,  semi-purulent  material.  I was  asked  to  see  the  patient 
with  Dr.  H.  O.  Long  and  Mr.  Bromley  on  14  April.  For  the  past 
three  days  he  had  suffered  intense  pain  in  the  right  lower  chest  and 


245 


TREATMENT  OF  STREPTOCOCCAL  FEVER 
right  shoulder,  and  was  looking  alarmingly  ill.  Pulse-rate  120; 
dyspnoea;  orthopnoea.  No  spleen  tumour.  No  diarrhoea.  A large 
effusion  was  located  at  the  right  base.  Leucocyte  count,  three  days 
previously  16,000  cells  per  c.nun.,  had  risen  to  25,000  cells  per 
c.mm.  He  had  received  two  injections  of  polyvalent  serum  and  two 
of  scarlatinal  antitoxin  and  one  dose  of  mercurochrome  intra- 
venously. Preparations  were  being  made  for  an  immuno-transfusion. 
In  view  of  the  definite  chest  localization,  the  absence  of  any  further 
septicaemic  signs,  and  the  good  leucocytosis,  I advised  against  any 
further  serum,  chemotherapy,  or  immuno-transfusion.  Needling  of 
the  chest  to  determine  the  nature  of  the  fluid  was  performed  on 
16  April,  8 oz.  of  turbid  fluid  being  withdrawn.  On  settling,  this 
showed  about  one  inch  of  pus  at  the  bottom  of  a full  test-tube. 
General  condition  satisfactory.  Fluids  taken  well.  Several  more 
needlings  were  carried  out,  and  each  time  the  sediment  of  pus  on 
standing  showed  a definite  increase.  On  23  April  a portion  of  the 
ninth  rib  was  resected  by  Mr.  Bromley,  and  one  and  a half  pints  of 
very  thick  fluid  with  flakes  of  pus  were  discharged.  Treatment  with 
closed  drainage.  Recovery  was  slow  and  tedious,  drainage  at  first 
not  very  satisfactory  and  the  wound  margin  became  infected.  In 
September  a secondary  operation  for  a persisting  sinus  was  performed, 
and  the  patient  was  subsequently  restored  to  health.  The  nature  of 
the  original  osteomyelitis  remains  undecided,  but  the  history  suggests 
that  this  case  may  have  been  another  example  of  a streptococcal 
superimposed  upon  a staphylococcal  Infection. 

Case  8.  Streptococcal  Fever  ( Septicaemia ) following  an  Infected 
Abrasion.  Death.  A hospital  sister,  aged  40,  returned  from  a holiday 
feeling  in  the  best  of  health  on  4 June  1929.  She  was  then  employed 
in  a very  heavy  ward  with  septic  cases.  On  11  June  she  had  a hot 
bath,  feeling  very  tired,  and  almost  immediately  began  to  feel  ill  and 
feverish,  but  had  no  rigor.  She  developed  severe  pain  in  the  right 
shoulder  and  down  the  arm,  and  later  pains  in  the  left  arm  and  both 
legs.  On  12  June  her  temperature  was  103®,  and  chemosis  of  both 
eyes  with  punctate  haemorrhages  in  the  lids  appeared.  There  was 
occasional  sickness,  but  no  diarrhoea.  Large  raised  erythematous 
patches  on  both  forearms,  slight  epistaxis,  and  a feeling  of  tightness 
in  the  chest  were  among  the  other  symptoms  noted.  I saw  her  on 
14  June,  and  found  her  very  ill,  with  dry,  dusky  red  pharynx  and 
blood  trickling  down  from  the  post-nasal  space.  There  was  also  a 
tiny  pustule  near  the  nail  bed  of  the  right  forefinger,  where  she  had 
experienced  slight  soreness  two  days  before  the  onset  of  her  illness. 
There  was  no  adenitis  or  lymphangitis.  Blood  cultures  grew  strep- 
tococci. Leucocyte  count  15,000.  Scarlatinal  antitoxin  was  given. 
Death  occurred  a few  days  later. 

Case  9.  Streptococcal  Fever  (Bacteriaemia)  following  an  infected 
Haematoma.  Becovery.  A fine,  vigorous,  healthy  aged  64, 


240  THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
bruised  his  left  leg  while  riding  through  a gate,  paid  no  attention  to 
the  injury,  and  went  to  o point-to-point  meeting  on  the  next  day. 
Extcnsh  e bruising  with  superficial  blebs  developed,  and  these  were 
opened.  Deeper  planes  became  infected,  and  the  wound  was  treated 
with  B.I.PJP.  lie  would  not  rest  properly,  and  some  superficial 
sloughing  occurred.  About  sixteen  days  after  the  injury  he  felt  seedy 
and  had  a solitary  rigor.  Streptococci  were  grown  from  the  wound 
and  the  blood-stream.  There  was  some  vomiting,  and  he  had  pain 
after  food.  The  temperature  hovered  between  102s  and  103%  but 
the  pulse-rate  was  not  proportionately  raised,  there  were  no  further 
rigors,  and  he  had  no  diarrhoea.  Some  cellulitis  around  the  wound 
and  lymphangitis  in  the  groin  were  next  observed.  I was  asked  to 
see  him  in  consultation  with  Dr.  F.  C.  Young  and  Mr.  J.  L.  Joyce 
at  the  end  of  the  third  week  from  the  injury  to  advise  in  regard  to 
prognosis  and  the  treatment  of  his  general  condition.  He  was  low 
and  depressed,  but  had  a good  pulse  not  exceeding  80  to  the  minute, 
his  skin  was  cool  and  the  spleen  was  not  palpable.  Leucocyte  count 
10,300.  I concluded  in  favour  of  a bacteriaemia,  and  for  tliis  reason 
gave  a favourable  prognosis,  and  advised  against  serum  therapy  or 
chemotherapy.  He  Iiad  a slow  convalescence  in  respect  of  the  local 
lesion,  but  made  a good  recovery. 

Case  10.  Streptococcal  Fever  (Septicaemia)  Jollmring  a Throat  Injec- 
tion and  Mastoiditis.  Septic  Arthritis  of  Ilip.  Recovery.  A previously 
healthy  little  girl,  aged  10,  bad  her  tons  Us  enucleated  in  the  middle 
of  March  1030.  Just  after  her  return  home  a virulent  streptococcic 
sore  throat  affected  all  the  members  of  her  household,  including 
herself.  She  developed  a left  otitis  media  and  mastoiditis  for  wliich 
a radical  operation  was  performed.  General  septicaemia  with  swing- 
ing pyrexia,  occasionally  as  high  as  105*  and  100%  with  rigors,  followed. 
There  was  also  meningism,  but  the  CJ5.F.  was  dear.  She  was  given 
antistreptococcic  serum  intrathecallv,  subcutaneously,  and  rec tally. 
The  spleen  became  enlarged,  and  I was  asked  to  see  her  with  Dr.  n.  E. 
Rawlence  and  Dr.  C.  Fiekcn  on  13  April  1030,  ten  days  after  the 
mastoid  operation.  I found  her  morale  good,  her  tongue  clean  and 
moist,  and  she  was  taldng  fluid  nourishment  and  sleeping  well.  The 
spleen  was  nearly  three  fingers  down  and  firm,  almost  hard  (compare 
Case  4,  in  wliich  by  the  time  the  spleen  was  large  and  hard  the  grave 
septicaemic  phase  had  passed).  Fain  had  just  appeared  in  the  left 
knee,  and  I found  swelling  around  the  left  hip-joint  which  was  very 
painful  to  move.  On  1 5 April  pain  in  the  hip  had  greatly  abated  and 
she  was  rather  better.  I was  called  to  see  her  agaia  on  23  April.  The 
pyrexial  curve  had  adopted  a lower  level,  hut  the  child  had  become 
very  wasted  and  anaemic.  Spleen  smaller.  In  the  last  forty -eight 
hours  the  left  leg  had  become  swollen,  an  evident  ‘white  leg’.  There 
was  some  glossitis.  On  each  occasion  I ventured  a good  prognosis 
as  regards  life.  At  this  time  the  haemoglobin  was  down  to  30  per 


217 


TREATMENT  OF  STREPTOCOCCAL  FEVER 
cent,  and  the  white  count  was  only  9,500  cells  per  c .mm.  A little  later 
the  left  hip  was  again  discovered  to  be  painful,  and  X-ray  examina- 
tion, which  had  revealed  no  abnormality  in  the  early  stages,  now 
showed  some  destruction  of  the  head  of  the  femur.  A plaster  ‘spica’ 
was  applied.  The  general  condition  subsequently  improved  steadily, 
but  the  prospects  of  full  functional  recovery  in  the  joint  seemed  poor. 

Case  11.  Streptococcal  Fever  {Septicaemia).  Meningitis.  Death.  A 
girl,  aged  13,  with  a history  of  otitis  media  and  mastoiditis  following 
tonsillitis  three  years  previously.  For  this  a radical  mastoid  operation 
and  later  tonsillectomy  had  been  performed.  Thereafter  she  enjoyed 
good  health  until  19  May  1930,  when,  in  the  course  of  an  epidemic  of 
tonsillitis  at  her  school,  she  was  taken  suddenly  ill  with  high  fever. 
The  temperature  reached  105°  on  the  first  day.  There  was  no  com- 
plaint of  sore  throat  and  no  visible  pharyngitis,  no  cervical  adenitis, 
no  splenic  enlargement,  and  during  the  first  three  days  she  was  very 
little  inconvenienced  by  her  high  pyrexia.  On  the  third  day  a 
streptococcus,  haemolytic  but  described  as  *not  strongly  so’,  was 
grown  from  the  blood.  She  was  given  10  c.c.  of  scarlatinal  antitoxin, 
and  on  each  of  the  three  ensuing  days  15  c.c.  of  polyvalent  antistrep- 
tococcic serum.  Her  temperature  then  fell  suddenly  to  subnormal 
and  her  pulse-rate  from  110  to  76.  Two  more  doses  of  polyvalent 
serum  (15  c.c.)  were  given,  each  time  intravenously.  On  the  next  day 
the  temperature  rose  again  as  suddenly  to  105°  and  the  pulse-rate  to 
120  and  130.  I was  asked  to  see  her  at  this  point,  on  the  seventh  day. 
In  the  past  twenty-four  hours  she  had  developed  left-sided  headache 
and  a droop  in  the  left  upper  eyelid.  She  was  clear  mentally,  had  a 
clean  tongue  and  a moist  skin,  but  was  very  gravely  ill.  The  most 
disconcerting  findings  were  a very  slight  neck-rigidity  and  Kernfg’s 
sign.  There  were  no  symptoms  or  signs  of  middle-car  disease.  On 
the  eighth  day  the  temperature  was  105-4°,  respirations  30.  I advised 
against  any  further  serum  therapy.  Lumbar  puncture  on  the  tenth 
day  gave  slightly  turbid  fluid  under  increased  pressure.  Blood  culture 
now  sterile.  Leucocytes  only  7,500  per  o.mm.  with  80  per  cent, 
polymorphonuclear  cells.  Serum  given  intrathecally.  On  the  eleventh 
day  signs  of  a right  hemiplegia  appeared,  becoming  complete  on  the 
twelfth  day,  when  coma  and  Cheyne-Stokes  breathing  were  recorded 
and  death  closed  the  scene. 

(c)  Prognosis 

Death  occurred  in  one-third  of  this  small  series,  in  one 
case  on  the  fourth,  in  one  on  the  seventh,  and  in  one  on 
the  twelfth  day.  It  may  be  generally  accepted  that  those 
patients  who  survive  the  first  onslaught  and  weather  the 
first  fortnight  have  a very  fair  prospect  of  recovery  even 
when  high  pyrexia  continues  and  complications  ensue. 


248  Tim  NATURAL  HISTORY,  PROGNOSIS,  AND 
Within  the  first  fortnight,  in  other  words,  it  is  commonly 
decided  whether  the  fight  is  to  be  a winning  or  a losing  fight, 
and  whether  the  infection  is  to  be  driven  from  the  genera! 
circulation  into  local  strongholds.  If  the  infection  is  massive 
or  resistance  poor,  exhaustion  or  some  grave  complication 
such  as  pericarditis  or  meningitis  will  probably  prove  fatal 
before  two  weeks  have  passed.  If  the  infection  is  less  heavy 
or  resistance  good  or  at  least  more  evenly  weighted  against 
the  invader,  the  general  defence  mechanisms  will  have  been 
mobilized  by  this  time.  By  this  time  too  metastatic  infec- 
tions, which  sometimes  improve  prognosis  rather  than 
otherwise,  will  be  making  their  appearance.  In  two  of  the 
three  fatal  cases  described  there  was  no  evident  focus  of 
invasion.  In  two  no  evident  metastasis  occurred.  In  the 
third  the  very  fatal  complication  of  meningitis  was  the 
cause  of  death  at  a time  when  organisms  were  no  longer 
recoverable  from  the  blood.  All  three  patients  were  young. 
One  was  probably  infected  initially  by  influenza ; one  was 
a sister  in  charge  of  a heavy  septic  ward ; the  third  acquired 
a rapid  general  infection  through  the  throat  during  a school 
epidemic  of  tonsillitis  and  established  no  lymphatic  defence. 
Cases  10  and  11  remind  us  of  the  occasional  disadvantage  of 
being  deprived  of  all  tonsillar  tissue.  In  the  second  and 
third  of  the  fatal  cases  the  leucocyte  counts  were  respec- 
tively 15,000  and  7,500  cells  per  c.mm.  The  leucocyte 
counts  in  five  of  the  cases  which  recovered  were  25,000; 
21,000;  19,000;  10,650;  and  9,500.  Metastatic  fixation  in 
joints  occurred  in  each  of  the  two  last  with  low  counts  and 
in  the  pleura  in  the  case  with  the  highest  count. 

The  following  points  may  be  said  to  favour  a good 
prognosis:  (1)  a surgically  accessible  focus  of  invasion;  (2) 
survival  beyond  the  immediate  stage  of  onslaught,  i.e. 
beyond  the  first  fortnight;  (3)  a high  leucocytosis;  and  (4) 
favourable  localizations  amenable  to  surgical  treatment. 
Unfavourable  localizations  are  those  involving  the  meninges 
and  the  pericardium.  Blood-borne  infections  of  the  peri- 
toneum are  also  unfavourable. 

It  has  always  been  recognized  that  surgeons’  wounds  and 
puerperal  septicaemia  carry  a particularly  grave  risk.  In  the 


TREATMENT  OF  STREPTOCOCCAL  FEVER  249 
first  instance  this  probably  depends  on  the  virulence  of  the 
infecting  strain,  perhaps  immediately  enhanced  by  ‘passage’. 
In  the  second  preceding  anaemia  and  exhaustion,  the  extent 
and  seclusion  of  the  raw  infected  areas,  and  the  readiness 
with  which  infection  may  be  spread  and  absorbed  in  the 
pelvis  play  their  inevitable  part,  and  the  infecting  strain  is 
all  too  frequently  a haemolytic  streptococcus. 

(d)  Treatment 

The  same  general  principles  of  non-specific  treatment 
outlined  for  Staphylococcal  Fever  may  be  held  to  apply  in 
Streptococcal  Fever.  They  include  (1)  good  nursing;  (2)  a 
copious  fluid  intake  up  to  six  pints  and  more  in  the  day, 
together  with  glucose  and  alkalis  during  the  invasion  stage 
when  the  heart  is  severely  taxed  and  febrile  acidosis  and 
vomiting  are  commonly  present ; (8)  watchful  care  for  the 
development  of  infection  in  the  cellular  tissues,  joints,  pleura, 
and  pericardium,  effusions  being  treated  so  far  as  possible  by 
timely  aspirations  so  long  as  the  fluid  remains  thin,  and  by 
surgical  drainage  if  it  becomes  frankly  purulent.  Wien 
blood  cultures  become  negative,  but  the  temperature  re- 
mains high,  the  search  for  metastases  must  be  pursued  with 
particular  care;  (4)  morphine  for  pain,  restlessness,  and 
sleeplessness ; and  (5)  appropriate  immobilization  of  infected 
joints.  The  older  antiseptics  by  the  intravenous  route  are 
to  be  avoided.  There  is  no  sound  evidence,  whether  experi* 
mental  or  clinical,  that  they  do  good.  Some  of  them  have 
undoubted  toxic  effects.  Their  administration  can  be 
distressing  to  the  patient  and  they  are  capable  of  causing 
disturbing  symptoms.  The  failure  of  local  antiseptics  in 
infected  wounds  has  long  been  proved  and,  surely,  in 
generalized  infection  general  antisepsis  is  less  rather  than 
more  likely  to  succeed.  Whether  or  not  the  administration 
of  antistreptococcic  serum  is  ever  a cause  of  improve- 
ment or  recovery  is  also  open  to  debate.  In  a given  case  we 
have  no  certainty  that  the  sera  available  are  specific  for  the 
particular  invading  organism.  It  is  not  proved  that  any 
of  the  available  sera  are  strictly  anti -bacterial.  Some  of 
them  are,  however,  reputed  to  be  antitoxic,  and  note- 


250  NATURAL  HISTORY  OF  STREPTOCOCCAL  FEVER 
worthy  among  them  is  scarlatinal  antitoxin,  upon  which 
good  reports  have  been  published  from  time  to  time  both 
in  scarlet  fever  and  other  streptococcal  infections.  On  the 
whole,  we  must  confess  that  there  was  never  any  strong 
evidence  in  favour  of  the  efficacy  of  serum  therapy.  It  was 
very  generally  employed  for  many  years,  and  hod  its  results 
been  in  any  way  dramatic,  there  would  have  been  a weightier 
consensusof  opinion  in  support  of  it.  Anaphylactic  symptoms 
were  a frequent  and  sometimes  a grave  disadvantage.  I 
have  had  the  experience  of  being  called  to  a case  of  serum 
sickness  so  severe  and  crippling  as  to  suggest  that  the  patient 
had  entered  on  a new  phase  of  the  original  septic  infection 
for  which  the  scrum  had  been  given. 

But  in  any  case  sulphonamidcs  nnd  penicillin  have  now 
abolished  the  need  for  the  use  of  antiseptics  and  sera,  nnd 
have  greatly  reduced  mortality  and  diminished  the  tale  of 
local  complications.  While  the  benefits  of  modem  chemo- 
therapy can  be  no  more  disputed  than  the  malarial 
chemotherapies,  it  is  a pity  that  there  are  no  reliable 
figures  of  mortality,  end-results,  and  the  incidence  of  main 
complications  by  which  to  effect  comparisons  of  treatment 
‘then  and  now’. 

Fresh  air  and  sunshine  and  appropriate  treatment  of 
anaemia  as  soon  as  possible  after  the  acute  phase  is  passed 
continue  to  play  the  same  useful  role  which  they  arc  known 
to  play  in  other  bacterial  diseases. 


xvm 


THE  NATURAL  HISTORY,  PROGNOSIS,  AND 
TREATMENT  OF  INFECTIONS  WITH 
BACILLUS  COLI  COMMUNIS 
In  the  foregoing  lectures  I have  considered  the  clinical 
consequences  of  staphylococcal  and  streptococcal  infections 
respectively.  In  each  I made  it  my  endeavour,  largely  on  a 
basis  of  personal  records  and  experience,  to  sketch  the  whole 
natural  history  of  the  disease  in  question,  just  as  one  might 
depict  the  natural  history  of  typhoid  fever,  lobar  pneumonia, 
or  any  other  specific  malady.  By  too  much  concentration 
on  the  local  effects,  the  surgical  aspects,  or  the  bacterio- 
logical characters  of  the  septic  fevers  and  by  a neglect  of 
‘the  general  view’  it  seemed  to  me  that  we  were  sometimes 
liable  to  a loss  of  judgement  in  our  approach  to  the  practical 
problems  connected  with  their  aetiology,  prognosis,  and 
treatment.  Starting  with  the  local  lesion  or  invasion  the 
varieties  of  general  dissemination  which  may  follow,  leading 
on  the  one  hand  to  a more  or  less  benign  bacteriaemia,  and 
on  the  other  to  a grave  septicaemia  or  pyaemia,  were  in  turn 
reviewed.  For  each  of  the  septic  fevers  certain  sites  of 
election  in  respect  of  metastasis  or  residual  settlement  are 
discovered  which  give  character  to  the  disease  and  are 
therefore  helpful  in  diagnosis.  Thus  in  the  case  of  staphy- 
lococcal fever  metastases  show  a selective  affinity  for  the 
bones  in  childhood  and  for  the  renal  cortex  and  the  prostate 
in  adult  life,  although  we  find  that  they  may  also  appear 
in  skin,  muscle,  lung,  and  brain.  In  the  case  of  streptococcal 
fever  the  joints  and  serous  cavities  are  chiefly  involved. 
These  preferences  on  the  part  of  bacteria  for  different  anato- 
mical sites  might  well  suggest  fresh  avenues  of  inquiry  to 
the  bacteriologist  in  his  studies  of  microbic  biology.  There 
must  be  some  good  reason  why  the  septic  organisms  show 
such  individual  preferences ; why  the  pneumococcus  prefers 
the  lung,  and  the  meningococcus  the  meninges,  notwith- 
standing that  both  have  their  portal  of  entry  in  the  upper 


252  NATURAL  HISTORY,  PROGNOSIS,  AND  TREATMENT 
respiratory  tract ; and  why  organisms  of  the  typhoid  group 
and  the  colon  bacillus,  having  entered  and  left  the  circula- 
tion, prefer  to  colonize  the  urinary  and  biliary  passages. 

In  the  present  paper  I am  concerned  with  the  wanderings 
of  the  last-named  organism  when  it  invades  tissues  beyond 
the  bowel-wall,  and  more  especially  with  the  clinical  features 
of  these  invasions. 

Infection  with  the  colon  bacillus  is  usually  held  to  imply 
a simple  pyelitis  or  cystitis.  While  it  is  true  that  the  renal 
pelvis  and  the  bladder  are  the  commonest  sites  of  residual 
infection,  they  are  by  no  means  the  only  sites,  and  it  should 
not  be  forgotten  that  the  urinary’  infection  is  only  one 
episode  in  the  natural  history’  of  the  disease. 

Generalized  and  metastatic  infections  with  this  organism, 
while  prevalent  and  a frequent  cause  of  acute  and  chronic 
ill  health,  do  not  carry’  the  serious  menace  to  life  wliich  we 
associate  with  the  septic  fevers.  Indeed,  in  the  absence  of 
associated  pathologies,  such  as  obstructive  lesions  in  the 
urinary  tract  or  other  renal  damage,  it  may  be  doubted 
whether  they  are  ever  immediately  fatal. 

Aetiology  and  Paths  of  Invasion 

It  is  well  known  that  women  are  far  more  predisposed  to 
bacilluria  than  men,  and  that  pregnancy  increases  this 
liability.  In  my  own  experience  it  is  particularly  the  dark 
and  sallow  women  of  hyposthenic  habit  who  arc  afflicted ; 
that  is  to  say  women  endowed  with  the  particular  con- 
stitutional traits  which  we  have  come  to  associate  with 
intestinal  sluggishness.  It  must  be  relatively  rare  to 
encounter  the  disease  in  persons  of  robust  physique  and 
endowed  with  healthy  complexions  and  a regular  bowel 
function.  An  access  of  constipation  due  to  pregnancy  or 
illness,  abuse  of  purgatives,  and  particularly  such  condi- 
tions as  fatigue  or  ebilJ  or  a menstrual  period  are  often  the 
determining  factors.  There  is  a group  of  cases,  with  which 
others  must  also  be  familiar,  in  which  young  and  very 
recently  married  women  are  the  victims,  independently  of  a 
pregnancy.  Pyelitis  and  cystitis  may,  however,  occur  at  any 
age.  Among  children  girls  are  more  prone  to  bacilluria  than 


OF  INFECTIONS  WITH  BACILLUS  COLI  COMMUNIS  253 
boys.  Among  53  private  cases  of  pyelitis,  cystitis,  and 
bacilluria  I have  notes  of  40  females  and  13  males.  In 
men  (apart  from  prostatic  disease)  I chiefly  recollect  these 
infections  as  a consequence  of  enforced  rest  following  an 
operation  or  of  typhoid  fever  or  some  other  severe  illness. 
"Whether  in  the  case  of  typhoid  fever  the  permeability  of 
the  intestinal  mucosa  is  increased  by  local  ulceration,  or 
whether  a secondary  constipation,  a long  sojourn  in  bed, 
and  lowered  general  resistance  are  the  more  to  blame  it  is 
difficult  to  say.  As  pyelitis  usually  complicates  early  conva- 
lescence, the  second  view  is  perhaps  the  more  plausible. 

It  is  commonly  agreed  that  the  infection  derives  from  the 
bowel  where  the  colon  bacillus  is  a normal  inhabitant,  but 
various  theories  have  been  advanced  in  regard  to  the  actual 
paths  of  spread.  These  include  the  theory  that  organisms 
ascend  via  the  bladder.  While  a per-urethral  infection  in 
women  and  girls  is  a possibility,  in  the  male  it  is  anatomi- 
cally improbable,  and  in  either  sex  it  seems  unlikely  that 
infection  should  advance  ‘against  the  stream’  and  so  attack 
the  renal  pelvis.  Nor  is  this  the  order  of  events  if  we  may 
judge  by  the  clinical  histories  of  cases  of  pyelitis.  Ascent 
by  the  peri-ureteric  lymphatics  is  another  hypothesis  and 
trans-peritoneal  infection  of  the  kidney  a third  and,  to  my 
mind,  the  least  probable  of  all.  A typical  first  attack  of 
pyelitis  (or,  as  I should  prefer  to  call  it,  of  bacillaemia  with 
pyelitis)  starts  with  general  malaise,  headache,  fever,  vomit- 
ing, chilliness  or  actual  rigor,  pain  in  the  loin,  and,  generally 
a few  hours  later,  frequency  and  dysuria.  The  temperature 
may  rise  to  103°  or  more  and  the  aspect  of  the  patient  is 
that  of  a general  rather  than  a local  infection.  Furthermore, 
there  are  other  organs  besides  the  kidney  which  may  be 
affected  separately  or  simultaneously,  immediately  or  sub- 
sequently. Of  these  the  gall-bladder  and  its  ducts  are  the 
most  important.  Thus  clinical  observations  strongly  favour 
the  view  that  the  initial  infection  is  blood-borne  and  that  the 
urinary  and  biliary  tracts  only  become  involved  during  the 
excretion  of  organisms.  The  phase  of  bacillaemia,  however, 
is  of  short  duration,  perhaps  hours  only,  and  rarely  or  never 
days  as  in  the  bacteriaemic  or  septicaemic  phases  of  the 


254  NATURAL  HISTORY,  PROGNOSIS,  AND  TREATMENT 
septic  fevers.  Bacillaemia  probably  ends  when  the  bacilluria 
begins.  It  is  not  improbable  that  routine  blood  cultures 
in  the  early  stage  of  high  fever  and  rigor  in  cases  of  pyelitis 
would  give  positive  results.  Kidd  [1],  who  has  strongly 
advocated  the  hacmatogenous  theory,  and  Panton  and 
Tidy  [2]  have  actually  recorded  positive  blood  cultures  in 
a few  cases  during  or  near  the  stage  of  rigor,  but  it  should 
be  noted  that  their  cases  were  not  uncomplicated  cases  of 
pyelitis.  If  the  urinary  outflow  is  impeded  {vide  Case  G) 
the  bacillaemia  may  undoubtedly  persist.  It  is  possible  also 
that  re-infection  of  the  blood-stream  from  the  kidney  or 
lower  urinary  tract  may  occur.  Bactcriacmia,  with  or  with- 
out rigor,  has  been  shown  by  Barrington  and  Wright  [3] 
to  follow  operations  on  the  urethra,  and  is  the  probable 
explanation  of  ‘catheter- fever’,  which  closely  resembles  the 
prodromal  stage  of  a pyelitis. 

The  residual  infections  which  succeed  the  bacillaemia 
may  involve  the  pelvis  of  one  or  both  kidneys,  the  bladder, 
the  gall-bladder  and  bile-ducts,  the  prostate  gland,  or  the 
testicle.  Occasionally  two  or  more  of  these  organs  arc 
simultaneously  inflamed.  Where  the  kidney  is  concerned 
it  can  generally  be  assumed  that  the  inflammation  is  con- 
fined to  the  pelvis  and  calyces,  but  in  the  presence  of 
obstructive  lesions  a pyelitis  can  proceed  to  a pyclo-nephritis 
or  a pyo-nephrosis.  The  cholecystitis  also  is,  as  a rule, 
simple  or  non-suppurative,  and  the  same  may  be  said  of  the 
orchitis.  With  each  organ  the  natural  tendency  is  to  a 
rapid  subsidence  of  the  acute  inflammation  with  rest  and 
appropriate  treatment.  There  is,  however,  both  in  the 
biliary  and  in  the  urinary  tracts,  a strong  subsequent 
tendency  to  persistent  low-grade  infection  either  without 
symptoms  or  with  vague  impairment  of  health  and  oc- 
casional sharp  recurrences.  The  most  severe  initial  illness 
may,  however,  be  followed  by  complete  and  lasting  recovery. 

Clinical  Features  and  Course 
(1)  The  Urinary  Infections 

These  can  best  be  illustrated  by  the  histories  of  a few 
cases  of  varying  type  and  severity.  We  may,  however,  add 


OF  INFECTIONS  ’WITH  BACILLUS  COLI  COMMUNIS  255 
to  the  brief  description  of  symptoms  outlined  above  that 
there  is  commonly  very  considerable  malaise  and  prostra- 
tion for  the  first  few  days;  that  vomiting  and  abdominal 
pain,  sometimes  with  distension,  are  frequent ; that  palpa- 
tion of  one  or  both  of  the  kidneys  may  give  pain,  but  that 
there  is  not  usually  an  appreciable  enlargement  of  these 
organs;  and  that  micturition,  owing  to  the  cystitis,  is 
frequent  and  accompanied  by  burning  or  scalding  especially 
at  the  end  of  the  act.  The  urine,  when  held  up  to  the  light 
and  shaken  in  a test-tube,  is  seen  to  be  turbid  and  shimmer- 
ing. Given  a fresh  specimen  this  ‘shimmering’  is  a most 
useful  diagnostic  sign  in  cases  of  obscure  fever  or  dysuria 
(vide  Case  3).  In  some  cases,  and  especially  in  the  chronic 
phase  and  after  standing,  the  urine  gives  the  well-known 
‘fishy’  odour.  The  reaction  of  the  urine  is  strongly  acid. 
Albumin  is  present  but  usually  in  slight  amount  only. 
Some  cases  display  a frank  haematuria  for  a brief  period. 
The  centrifugalized  deposit  under  the  microscope  shows 
countless  pus  cells  and  organisms.  With  early  diagnosis  and 
appropriate  treatment,  including  alkaline  therapy,  the  tem- 
perature declines  rapidly  by  lysis  in  a few  days  and  only 
rarely  persists  for  more  than  a week.  Defervescence  is 
commonly  complete  soon  after  the  urine  becomes  alkaline. 
Anaemia  is  not  a feature  of  bacilluria,  but  a coexistent 
anaemia  due  to  another  cause  may  help  to  perpetuate 
infection.  Relapse  and  chronic  bacilluria  will  be  discussed 
in  more  detail  under  Prognosis. 

(2)  The  Biliary  Infections 

Cholecystitis,  with  which  in  the  more  chronic  cases  a mild 
degree  of  cholangitis  and  hepatitis  are  probably  associated, 
is  more  insidious  in  its  arrival  than  the  urinary  tract  infec- 
tions. Subacute  attacks  with  a ‘spike*  of  pyrexia,  nausea, 
right  subcostal  or  mid-epigastric  pain  and  tenderness,  and 
pain  referred  to  the  right  scapular  angle  are  the  common 
clinical  manifestations.  To  such  cases  the  label  of  ‘gastric 
influenza*  is  very  commonly  applied.  Many  of  the  cases 
are  seen  between  attacks  for  dyspeptic  symptoms,  of  which 
nausea,  epigastric  soreness,  and  flatulence  are  the  more 


250  NATURAL  HISTORY,  PROGNOSIS,  AND  TREATMENT 
prominent.  The  patients  are  sallow  and  pale  and  they 
may  acquire  with  the  passage  of  years  the  muddy  com- 
plexion which  is  customarily  ascribed  to  * intestinal  toxae- 
mia*, but  which  may  be  observed  in  other  varieties  of 
hepatic  disease.  There  may  be  slight  persistent  tempera- 
tures of  99°  or  thereabouts.  Occasionally  a pale  stool  or 
loose  motions  nre  noted.  Jaundice  is  not  frequent,  and 
major  biliary  colic,  unless  stones  arc  present,  is  also  rare. 
The  epigastric  discomforts  have  no  precise  relationship  to 
meals  and  the  nausea  is  continuous  or  comes  ‘in  waves’  and 
without  a special  morning  incidence  as  in  gastritis  and 
pregnancy.  Examination  shows  no  enlargement  of  the  gall- 
bladder. There  may  be  slight  flinching  or  guarding  on 
palpation  over  the  right  upper  quadrant  of  the  abdomen, 
and  tenderness  during  a deep  breath  at  the  gall-bladder 
point  is  usual,  but  varies  in  degree  with  the  activity  of  the 
inflammatory  process.  Some  cases  show  referred  tenderness 
over  the  middle  dorsal  spines.  The  age  incidence  of  simple 
cholecystitis  lies  especially  in  the  second  and  third  decades 
and  women  provide  the  majority  of  the  coses.  The  physical 
type  afflicted  is  again  the  costive,  hyposthenic  type.  By 
these  features  it  may  be  distinguished  from  the  stouter  and 
more  robust  type,  with  deep  chest  and  broad  epigastric 
angle,  which  we  have  come  to  associate  in  the  fourth  or 
fifth  decade  with  cholelithiasis. 


Case  Reports 

Case  I.  Simple  recurrent  pyelitis  and  cystitis.  A young  married 
woman,  who  gave  a history  of  o short,  sharp  attack  of  pyelitis  in  the 
seventh  month  of  a pregnancy  8 years  previously,  was  troubled  one 
day  with  slight  frequency  and  fever.  Against  advice  she  did  not  keep 
to  her  bed.  Dysuria  persisted  for  a week.  She  then  had  a solitary 
rigor  one  night  and  was  feverish  and  dully  throughout  the  next  day. 
At  the  time  of  examination  her  temperature  was  102®  (Chart  1); 
tongue  furred;  pain  in  the  loins.  A period  started  on  the  following 
day.  The  urine  was  ‘loaded*  with  pus  cells  and  B.  colt.  With  rest, 
liberal  fluids,  and  copious  alkalis  symptoms  rapidly  abated  and  the 
temperature  was  normal  by  the  fifth  day  of  treatment.  The  urine 
rapidly  became  clear  of  pus  cells  after  this  and  again  after  one  sub- 
sequent slighter  attack,  alkaline  therapy  being  employed  on  each 
occasion.  Three  years  later  the  patient  is  in  excellent  health. 


OF  INFECTIONS  WITH  BACILLUS  COLI  COMMUNIS  25T 
Case  2.  Acute  pyelitis  complicating  auricular  fibrillation.  Severe 
abdominal  pain.  A woman,  aged  54,  had  been  under  treatment  for 
auricular  fibrillation  with  pronounced  tachycardia  (i.e.  complete  rest 
and  digitalis)  during  a period  of  eleven  days.  She  then  complained  of 
a sudden  access  of  very  intense  abdominal  pain  which  she  was  unable 
to  locate  with  any  accuracy.  There  was  also  a complaint  of  pain  down 
the  left  leg,  but  this  was  transient.  She  looked  ill  and  was  unrespon- 
sive and  mentally  peculiar.  I noted  a vague  epigastric  tenderness  but 
no  rigidity  and  no  elevation  of  pulse-rate  or  temperature.  On  the 


next  day  the  temperature  rose  to  101°  in  the  evening  and  there  was 
tenderness  below  the  right  rib  margin.  The  urine  showed  albumin, 
copious  pus  cells,  with  an  occasional  red  cell,  and  was  highly  acid. 
The  pulse-rate,  which  had  been  recorded  at  ICO  before  digitalization 
and  which  had  fallen  to  88,  only  once  rose  above  92  during  the  period 
of  the  urinary  infection.  Alkaline  treatment  was  started  promptly 
with  immediate  alleviation  of  symptoms.  The  course  of  the  fever  is 
illustrated  by  Chart  2. 

Case  3.  Pyelitis  in  a child  causing  obscure  pyrexia.  A small  girl, 
aged  4}  years,  previously  lively  and  robust  and  of  healthy  parentage, 
had  been  ill  for  a fortnight  at  the  time  of  my  visit.  The  onset  of  her 
illness  had  been  abrupt  with  fever,  headache,  and  vomiting.  A 
swinging  pyrexia  varying  between  99®  in  the  morning  and  102®  or 
103®  in  the  evening  had  continued  ever  since.  Bowels  costive.  No 
chills  or  sweats.  Appetite  good.  There  had  been  complaint  of  dysuria 
on  one  occasion  only  and  there  was  no  frequency.  The  physical 
examination  was  entirely  negative.  Tuberculosis  and  typhoid  fever 
had  been  under  discussion.  On  shaking  a fresh  specimen  of  urine  in 


258  NATURAL  HISTORY,  PROGNOSIS,  AND  TREATMENT 
a test-tube  held  against  the  light  typical  shimmering  was  observed 
and  the  microscope  revealed  pus  cells  and  B.  coli.  There  was  a satis- 
factory response  to  alkaline  treatment. 

Case  4.  Acute  cholangitis,  pyelitis,  cystitis,  and  orchitis.  A medical 
man,  aged  35,  who  had  been  seriously  ill  with  acute  nephritis  in  1012, 
but  recovered  and  served  through  the  War,  was  subsequently  ex- 
plored on  account  of  gall-bladder  pain  in  1010.  lie  was  then  well 
until  February  1925,  when  he  became  ill  with  ‘influenzal’  symptoms 
and  took  to  his  bed  with  a temperature  of  101°.  Five  days  later 
nausea,  vomiting,  and  jaundice  were  added  to  his  symptoms.  lie  was 
ill  for  a fortnight  and  was  beginning  to  improve  when  he  developed 
follicular  tonsillitis  and  a simultaneous  dysuria.  I saw  him  with  n 
temperature  of  10 1°,  tenderness  in  the  gall-bladder  region,  a leucocyte 
count  of  21,000  cells  per  cm,  and  urine  loaded  with  pus  cells. 
He  was  admitted  to  hospital,  where  he  lay  gravely  ill  with  B.  coli 
pyelitis,  cystitis,  and  later  orchitis.  He  showed  no  response  to  urinary 
antiseptics,  but  improvement  followed  immediately  the  urine  was 
alkalinized.  He  was  given  vaccines  in  convalescence.  Recovery  was 
complete.  The  urine  became  perfectly  dear  and  has  remained  so 
since. 

The  two  cases  next  to  be  described  exemplify  effects 
which  may  follow  when  an  obstructive  factor  is  added  to 
infection.  In  the  first  case  (Case  5)  medical  treatment 
failed  repeatedly  to  relieve  symptoms.  In  the  second  case 
(Case  G)  blockage  of  the  ureter  by  a calculus,  in  association 
with  bacillaemia  and  pyelitis,  caused  a B.  coli  ‘septicaemia* 
with  very  grave  symptoms  which  were  quickly  relieved  after 
drainage  of  the  kidney.  By  the  lessons  of  Case  5 I have 
twice  been  enabled  to  recognize  from  the  history  the  pre- 
sence of  on  additional  mechanical  factor  complicating  infec- 
tion and  calling  for  surgical  relief. 

Case  5.  Chronic  pyelitis;  pyonephrosis.  A boy,  aged  18,  of  rather 
delicate  type,  had  been  liable  to  febrile  attacks  from  cliildhood. 
Eight  years  previously  infection  of  the  urinary  tract  with  B.  coli  bad 
been  diagnosed  and  for  3 years  he  had  recurring  attacks  of  fever  due 
to  this.  He  saw  various  specialists,  but  never  responded  to  treat- 
ment either  with  alkalis  or  antiseptics.  He  was  then  better  for  5 years. 
A month  before  I saw  him  in  consultation  with  Dr.  P.  L.  Richardson 
he  had  ngain  become  ill.  Further  consultations  had  been  held  before 
my  visit,  the  diagnosis  of  B.  coli  pyelitis  had  again  been  confirmed  by 
laboratory  inquiry,  and  the  usual  treatments,  including  alkalmizn- 
tion,  had  been  advised.  So  far  from  improving  his  condition,  treat- 
ment actually  appeared  to  make  him  worse  and  this  alone  was  so 


OF  INFECTIONS  WITH  B AC  ILL  VS  COLI  COMMUNIS  250 
unusual  as  to  make  me  suspicious  of  some  added  factor.  For  some 
days  his  temperature  had  been  rising  to  103°,  there  were  night-sweats, 
and  he  vomited  frequently.  In  this  illness  his  pain  and  tenderness 
had  been  confined  to  the  left  loin  and  there  was  no  dysuria — further 
points  in  favour  of  a localized  renal  trouble.  His  parents  were  acutely 
anxious  and  Dr.  Richardson  and  I were  therefore  agreeably  surprised 
to  find  them  radiant  on  our  arrival  "because  the  boy  had  ‘quite  sud- 
denly improved’  at  10  o’clock  that  morning  and  his  evening  tempera- 
ture was  down  to  09°.  This  sudden  improvement  again  suggested  to 
us  that  something  definite  and  dramatic  must  have  occurred  such  as 
the  release  of  a mechanical  block.  Hitherto  deep  palpation  had  been 
difficult  owing  to  tenderness,  but  I found  the  boy  so  much  more 
comfortable  that  I was  able  to  palpate  freely  in  the  left  loin  where  I 
convinced  myself  of  a slightly  enlarged  kidney.  I was  presented  with 
numerous  laboratory  reports  on  the  urine  all  pronouncing  in  favour 
of  D.  coli  pyelitis,  but  decided  that  I would  like  to  take  away  a speci- 
men with  me.  We  therefore  asked  the  boy  to  pass  water  in  our 
presence.  As  he  did  so  his  jaw  dropped  and  he  exclaimed,  * I’ve  never 
passed  anytliing  like  that  before’.  The  urine,  which  had  been  almost 
clear  in  the  rooming,  now  consisted  of  thick  creamy  pus.  He  had 
emptied  a pyonephrosis.  A 6hell  of  a kidney  was  removed  later  by 
Sir  John  Thomson-Walker  and  lie  made  a complete  recovery.  It  is 
evident  that  his  failure  to  respond  to  medical  treatment  had,  from 
the  beginning,  been  due  to  a partial  or  intermittent  obstruction  of 
the  left  ureter. 

Case  6.  B.  coli  septicaemia  xmlh  impacted  ureteric  calculus . A 
nervous  and  highly-strung  married  woman,  aged  85,  was  referred  to 
me  by  Mr.  Frank  Kidd,  under  whose  care  she  had  been  for  pyelitis, 
on  account  of  symptoms  referable  to  her  colon.  She  was  liable  on  the 
one  hand  to  spasmodic  bowel  pain  and  on  the  other  to  sudden  * chills’. 
Eighteen  months  later,  on  1 June  1930,  she  was  wakened  by  bad 
pain  in  the  lower  part  of  her  back,  became  ill  and  pyrexial,  and  com- 
plained of  pain  and  frequency.  The  pain  moved  to  the  left  side,  she 
had  frequent  rigors,  and  the  temperature  rose  to  100°  and  later  107°. 
The  onset  of  the  illness  coincided  with  a menstrual  period.  I saw  her 
In  consultation  with  Dr.  P.  W.  James  on  11  June.  She  was  mentally 
strange,  in  a typhoidal  state,  twitching,  incontinent,  and  drowsy. 
The  abdomen  was  soft  and  flaccid.  She  was  tender  in  both  flanks. 
She  was  passing  plenty  of  trrine.  The  leucocyte  count  was  1 7,300 
cells  per  c.mm.  with  90  per  cent,  of  polymorphonuclear  cells.  Blood 
culture  gave  a pure  growth  of  the  colon  bacillus.  On  14  June  Mr.  Kidd 
drained  the  left  kidney  which  was  full  of  foul  pus.  At  a later  operation 
he  removed  a stone  from  the  ureter,  and  she  made  good  recovery. 

It  is  probable,  as  Kidd  [1]  has  insisted  and  ns  has  been 
argued  above,  that  the  rigor-stage  of  B.  colt  infections 


200  NATURAL  HISTORY,  PROGNOSIS,  AND  TREATMENT 
represents  a true,  if  transient,  bacillaemia.  It  would  seem  to 
require  an  obstacle  to  natural  drainage  to  convert  a benign 
bactcriaemia  into  the  graver  state  which,  in  virtue  of  the 
hyperpyrexia  and  typhoidal  condition,  I have  here  ventured 
to  describe  as  B.  coli  septicaemia.  The  distinction  between 
a bactcriaemia  and  a septicaemia,  which  must  be  largely 
clinical,  I have  discussed  previously.1 

Case  7.  Infection  of  the  biliary  tract.  A young  woman,  aged  28, 
Jiad  a long  attack  of  catarehal  jaundice  as  a schoolgirl.  In  August 
1021  she  had  a sudden  bad  abdominal  pain  while  cycling.  Pain  per- 
sisted for  a day  or  two  but,  when  it  left  her,  she  remained  unwell  and 
was  in  bed  for  8 weeks  with  almost  constant  nausea,  poor  appetite, 
cold  extremities,  and  an  intermittent  pyrexia  of  00®  to  100®.  She 
lost  weight  considerably,  but  had  begun  to  improve  by  the  time  I 
saw  her.  Her  doctor  had  been  apprehensive  of  pulmonary  tubercu- 
losis. Of  this  I could  find  no  evidence.  She  was  sallow  and  pigmented 
and  the  blood-pressure  was  low.  There  was  tenderness  under  the  right 
rib-margin  during  inspiration.  I advised  dietary  measures,  exclusion 
of  eggs,  and  treatment  with  urotropine.  Her  health  steadily  im- 
proved. Two  years  later  her  weight  had  increased  by  more  than  a 
stone,  but  she  still  had  occasional  nausea  and  right  sub-scapular  pain. 

Other  cases  show  more  in  the  way  of  local  and  less  of 
general  symptoms,  and  there  is  considerable  variety  in  the 
clinical  pictures  which  may  be  seen  in  practice.  Simple 
cholecystitis,  which  is  due  to  the  colon  bacillus  in  the  great 
majority  of  cases,  is  also  probably  the  commonest  organic 
cause  of  chronic  dyspepsia  in  women. 

Differential  Diagnosis 

The  diagnosis  of  bacillaemia  with  acute  pyelitis  and 
cystitis  is  not,  as  a rule,  difficult.  Cases  of  right-sided 
pyelitis  with  severe  pain  may  simulate  appendicitis ; cases 
with  much  fever  and  few  localizing  symptoms  may  suggest 
a typhoid-group  infection;  and  cases  with  haematuria  may 
have  to  he  distinguished  from,  renal  calculus.  A careful 
history  and  a macroscopic  and  microscopic  examination  of 
the  urine  will  generally  decide.  In  the  chronic  phase  both 
pyelitis  and  cholecystitis  may  lead  to  fruitless  appen- 
dicectomy.  The  orchitis  may  be  erroneously  attributed  to 

* Vide  Lectures  XVI  and  XVII. 


OF  INFECTIONS  WITH  BACILL  VS  COL1  COMMUNIS  261 
gonococcal  or  other  infection.  The  general  malaise  and 
debility  and  the  slight  recurring  pyrexia  •which  characterize 
some  of  the  biliary  tract  infections  may  readily  create  appre- 
hension about  early  pulmonary  tuberculosis,  and  the  pain  of 
perihepatitis  in  such  cases  has  been  attributed  to  pleurisy. 
The  symptoms  of  acute  and  sub-acute  cholecystitis  are 
often  attributed  to  ‘gastric  influenza’. 

Prognosis 

As  indicated  above  the  prognosis  in  regard  to  life  in 
uncomplicated  cases  of  bacilluria  is  uniformly  good.  Where 
the  infection  complicates  old  age  or  a paraplegia  it  may 
hasten  the  end.  As  a complication  of  ureteric  blockage  or 
prostatic  enlargement  its  seriousness  has  been  fully  appre- 
ciated by  the  genito-urinary  surgeon  and,  in  the  latter  case, 
the  risks  of  renal  failure  are  known  to  be  much  increased. 

The  prognosis  with  regard  to  full  restitution  of  health  is 
always  somewhat  uncertain.  Many  cases,  it  is  true  (perhaps 
the  majority),  recover  completely  or,  as  in  Case  I,  enjoy  long 
spells  of  good  health.  Others  retain  a permanent  bacilluria 
and  a liability  to  recurrent  attacks  of  pyelitis  and  cystitis. 
Others  again  retain  a bacilluria  but  are  well.  A young  man 
of  my  acquaintance  has  had  a pyuria  evident  to  a naked-eye 
inspection  of  his  specimens  for  many  years  but  without 
any  untoward  symptoms.  These  chronic  bacilluric  cases 
are  very  resistant  to  treatment  whether  with  antiseptics, 
alkalis,  or  vaccines.  The  method  of  treatment  with  keto- 
genic  diets  at  one  time  seemed  to  offer  better  prospects 
of  success. 

I am  strongly  of  the  opinion  that  if  alkalinization  were 
complete  and  sufficiently  prolonged  in  the  first  instance 
there  would  be  fewer  cases  of  chronic  bacilluria.  Time  and 
zeaf  are  commonly  misspent  in  the  exhibition  of  antiseptics 
and  vaccines. 

With  the  biliary  tract  infections  there  is  the  same  liability 
to  relapse  and  chronicity  and  the  way  may  be  paved  for 
gall-stone  formation  in  later  life.  Early  diagnosis  and  active 
treatment  should  diminish  these  liabilities,  but  the  symptoms 
often  linger  unrecognized  for  years  and  long  perpetuation 


2C2  NATURAL  HISTORY,  PROGNOSIS,  AND  TREATMENT 
of  the  local  inflammatory  process  naturally  interferes  with 
successful  medication. 


Treatment 

The  treatment  of  acute  pyelitis  should  include  bed, 
warmth,  plentiful  barley-water,  fruit  drinks,  and  weak  tea, 
but  preferably  little  milk.  The  lower  bowel  should  be  cleared 
with  an  enema.  Full  doses  of  nlkalis,  in  the  form  of  potas- 
sium citrate  and  sodium  bicarbonate,  should  be  given  and 
the  amounts  rapidly  increased  until  each  specimen  of  urine 
passed  turns  red  litmus-paper  blue.  Tliirty  grains  of  potas- 
sium citrate  with  15  grains  of  sodium  bicarbonate  four- 
hourly  would  be  a reasonable  initial  dose,  but  much  more 
may  be  necessary,  and  I have  given  up  to  three  or  four 
hundred  grains  of  alkali  in  the  twenty-four  hours  to  a 
child  of  ten  or  twelve  before  atkalinization  was  complete. 
The  risk  of  causing  an  alkaline  intoxication  is  small.  As  a 
rule  the  temperature  drops  coincidentally  with  successful 
alkalinization  and  the  dysuria  is  quickly  alleviated.  It  was 
once  usual  to  follow  up  the  initial  alkalinization  with  a course 
of  urotropine  and  acid  sodium  phosphate,  but  thorough 
alkalinization  alone  is  very  effective  and  the  additional 
treatment  doubtfully  so.  Vaccines  were  also  employed  but 
should  play  no  part  in  the  treatment.  According  to  Shohl 
and  Janney  [4]  colon  bacilli  are  inhibited  from  growing  in 
urine  at  a pH  of  4*0  to  5*0  on  the  acid  side,  and  9*2  to  9’G  on 
the  alkaline  side,  and  the  ketogenic  diet  was  at  one  time 
in  favour.  Studies  by  Helmholz  and  Clark  [5]  reviewed 
by  Cabot  [G]  suggest  that  the  pH  of  the  urine  may  be 
sufficiently  raised  by  a ketogenic  diet  to  ensure  sterilization 
even  when  alkaline  and  antiseptic  treatments  have  com- 
pletely failed.  These  over-rich  diets  are  hard  to  tolerate  and 
by  some  patients  cannot  be  taken  at  all.  In  any  case  sul- 
phonamide  therapy  for  urinary  sterilization,  followinginitial 
symptomatic  relief  with  alkalis  has  superseded  these  meas- 
ures. With  milder  acute  attacks  the  patient  should  not  be 
kept  too  long  in  bed.  The  after-treatment  should  comprise 
a diet  liberal  in  fruit  and  fluids  and  rational  treatment  for 
constipation,  purgatives  being  forbidden.  Fatigue,  exposure 


OF  INFECTIONS  WITH  BACILLUS  C0L1  COMMUNIS  265 
to  cold,  and  the  approach  of  a menstrual  period  are  all  liable 
to  initiate  a relapse  and  patients  should  be  warned  of  this. 

’When  symptoms  are  resistant  to  routine  medicinal 
measures  and  there  is  unilateral  pain,  the  possibility  of  an 
obstructive  lesion  calling  for  surgical  relief  should  be  care- 
fully considered.  I have  avoided  separate  discussion  of 
bacillaemia  and  bacilluria  in  pregnancy.  The  treatment  of 
these  cases,  although  usually  conducted  on  similar  lines, 
may  on  occasion  call  for  special  experience  to  which  I can 
lay  no  claim. 

If  urotropine  is  of  doubtful  or  secondary  value  in  the 
urinary  infections  it  may  still  have  a place  in  the  treatment 
of  simple  cholecystitis.  In  these  cases  a morning  dose  of 
Epsom  salts  before  food  has  been  taken;  a mixture  con- 
taining 15  (increasing  to  30)  grains  of  urotropine  with  double 
the  dose  of  potassium  citrate  three  times  a day;  a diet  rich 
in  fruit  and  green  food  and  excluding  eggs;  liberal  fluids; 
prohibition  of  corsets;  and  regular  exercise — the  courses  of 
the  urotropine  being  repeated  at  intervals  for  a month  at 
a time — may  be  rewarded.  Hurst  recommended  much 
larger  doses  of  urotropine.  The  urine  must  be  kept  con- 
stantly alkaline  with  a view  to  avoiding  a chemical  cystitis. 
Many  patients  accept  the  value  of  the  rdgime  and  volun- 
tarily return  to  it  in  the  event  of  a recurrence  of  symptoms, 
but  it  is  difficult  to  decide  how  far  improvements  should  be 
attributed  to  the  urotropine  and  how  far  to  time  and  nature 
and  the  general  regimen.  Knott  [7]  has  shown  that  urotro- 
pine is  excreted  as  formaldehyde  in  the  bile  and  that  it  may 
exert  therein  an  inhibitory  effect  on  the  growth  of  organisms. 
Once  again  it  may  be  necessary  to  determine  the  presence 
or  absence  of  a mechanical  factor  in  the  shape  of  gall-stones. 
Surgery  should  only  be  sanctioned  in  simple  cholecystitis 
after  a very  careful  review  of  the  history  and  objective 
findings  and  when  medical  treatment  has  been  tried  and 
failed. 


Summary 

The  colon  bacillus  (a  normal  inhabitant  of  the  bowel),  in 
certain  constitutional  types  and  as  a result  of  certain  well- 


20  i INFECTIONS  WITH  BACILLUS  COLI  COMMUNIS 
recognized  disposing  causes,  may  enter  the  circulation.  A 
transient  bacillacmia  results  and  is  followed  during  the 
excretion  of  organisms  via  the  urinary  and  biliary  tracts 
by  pyelitis  and  cystitis,  or  by  cholecystitis.  Orchitis  and 
prostatitis  are  rarer  sequels.  Late  residual  infection  of  the 
renal  pelvis  and  bladder  or  of  the  gall-bladder  and  its 
ducts  is  common.  Adequate  treatment  with  full  alkaliniza- 
tion  in  the  early  stages  of  the  urinary  infections  gives 
satisfactory  results.  The  treatment  of  chronic  bacilluria  is 
less  satisfactory,  but  urinary  sterilization  with  sulphon- 
amides,  usually  quickly  accomplished  in  cases  of  short  dura- 
tion, is  also  effective  in  those  of  long  standing.  A tendency 
to  recurrence,  however,  may  persist.  In  the  early  and 
milder  biliary  tract  infections  morning  salts  and  disinfec- 
tion with  urotropine  have  been  held  to  be  effective.  In  a 
minority  of  both  the  renal  and  biliary  cases  medical  treat- 
ment is  rendered  unavailing  by  an  added  obstructive  or 
mechanical  factor,  the  presence  of  which  can  often  be 
appreciated  by  a careful  attention  to  historical  detail  and 
symptoms.  In  these  cases  surgical  treatment  is  appropriate. 

A wider  appreciation  of  the  importance  of  a healthy  bowel 
and  avoidance  of  the  purgative  habit  would  probably  do 
more  to  diminish  the  incidence  of  these  prevalent  infections 
than  any  other  single  measure. 

REFERENCES 

1.  Kidd,  F.:  Common  Infections  of  the  Kidneys.  London,  1020. 

2.  Panton,  P.  N.,  and  Tidy,  H.  L.:  Lancet,  1012,  ii.  1500. 

3.  Barrington,  F.  J.  F.,  and  Wright,  IL  D.:  Joum.  Path,  and  Bad., 

1930,  xxxiii.  871. 

4.  Suohl,  A.  T.t  and  Jassey,  J.  H.i  Joum.  Urol.,  1017,  i.  211. 

5.  IIeluiiolz,  H.  F.,  and  Clark,  A.  L.:  Prof.  Staff  Meetings,  Mayo 

Clinic,  1031,  vi.  605. 

6.  Cabot,  H.:  Lancet,  1032,  i.  1038. 

7.  Knott,  F.  A.:  Guy's  llosp.  Hep.,  1023,  lxxiii.  105. 


20G  THE  PROGNOSIS  AND  TREATMENT  OF 
follows.  We  need  to  know  how  far  it  is  now  incumbent  upon 
us  to  consider  the  employment  of  serum  in  lobar  pneumonia 
as  a routine,  or  if  this  is  not  warranted,  how  we  should  select 
the  cases  to  be  so  treated.  Recognizing  that  the  method 
calls  for  experience  and  considerable  technical  skill  we  also 
need  to  know  whether  cases  can  be  adequately  handled  in 
the  home  and,  if  not,  whether  they  ought  to  be  moved  to 
hospital  in  face  of  the  belief  that,  given  good  conditions, 
the  avoidance  of  such  a transfer  generally  provides  a better 
prospect  of  recovery. 

It  is  a main  purpose  of  this  communication  to  seek  an 
answer  to  these  questions.  My  personal  experience  of  serum 
therapy  in  pneumonia  is  negligible,  but  I have  long  been 
interested  in  the  natural  history  of  the  disease,  and  it  was 
my  good  fortune  to  be  a participant  in  the  discussion  on 
serum  treatment  arranged  by  the  British  Medical  Asso- 
ciation in  1932.  I have  also  had  the  pleasure  of  meeting 
several  of  the  leading  British  and  American  investigators 
and  of  serving  on  committees  which  are  closely  concerned 
with,  the  problem. 

There  have  been  discoveries  in  the  scientific  treatment  of 
disease  in  recent  years  which  have  been  promptly  accepted 
and  universally  applied,  so  apparent  and  remarkable  were 
their  achievements.  Of  such  are  insulin  in  diabetes  and 
liver  treatment  in  pernicious  anaemia.  The  anti-pneumo- 
coccal  sera,  also  due  to  careful  scientific  studies,  arc,  how- 
ever, in  a different  category  and  for  various  reasons  have 
produced  no  such  dramatic  change  in  practice.  They  de- 
mand special  care  and  experience  for  their  administration ; 
their  preparation  is  costly ; they  show  n limited  specificity ; 
it  is  very  difficult  to  assess  the  several  causes  of  symptoms 
and  mortality  in  the  disease  which  they  are  intended  to 
benefit;  and,  finally,  this  disease  has  already  a high  natural 
recovery-rate.  We  are  not  entitled  to  conclude  from  this 
that  sera  will  fmd  no  established  place  in  our  therapeutic 
armoury.  Rather  should  we  seek  to  determine  the  scope 
and  limits  of  their  utility. 

Now  we  cannot  discuss  the  merits  of  a new  remedy 
unless  we  have  a just  appreciation  of  the  natural  morbidity 


LOBAR  PNEUMONIA  2G7 

and  mortality  of  the  disease  which  it  is  purported  to  relieve 
or  cure.  For  this  reason  I must  ask  attention  first  of  all  to 
the  difficult  matter  of  prognosis  in  pneumonia — that  is  to 
say,  of  pneumonia  when  left  to  nature  and  the  nurse.  There- 
after, having  briefly  reviewed  the  contributions  of  non- 
specific therapy  and  the  methods  and  results  of  serum 
therapy,  I shall  attempt  an  estimate  of  the  extent  to  which 
we  should  be  prepared  to  modify  practice  on  the  basis  of  the 
newer  knowledge. 

Mortality  and  Prognosis 

As  has  been  implied,  we  cannot  claim  that  we  are  able 
to  reduce  the  mortality  or  alter  the  morbidity  of  a disease 
until  we  know  what  its  mortality  and  morbidity  are.  When, 
as  in  the  case  of  pneumonia,  these  vary  in  some  degree  from 
year  to  year,  very  considerably  from  country  to  country, 
and  markedly  so  in  relation  to  age,  social  environment, 
individual  constitutional  factors,  and  the  type  of  invading 
organism,  our  difficulties  become  very  complex.  Both  the 
prevalence  and  mortality  of  pneumonia  in  the  United  States, 
where  the  bulk  of  the  work  on  serum  therapy  has  been  done, 
are  more  serious  than  in  this  country  and  to  some  extent 
our  conclusions  must  be  drawn  anew. 

At  present  we  have  hospital  figures  in  England  and 
Scotland  which  show  that  the  mortality  of  lobar  pneumonia 
lies  somewhere  between  10  and  20  per  cent.  Waterfield  [I], 
investigating  the  figures  at  Guy’s  Hospital  over  a nine-year 
period  ending  in  1930,  found  a total  mortality  of  1G  per 
cent,  between  the  ages  of  13  and  75  years.  One- third  of  the 
deaths  occurred  over  the  age  of  50.  There  were  no  deaths 
between  the  ages  of  15  and  20.  We  have  no  exact  figures 
as  to  the  mortality  of  patients  treated  in  their  homes,  and  I 
imagine  that  many  more  patients  in  this  country  am  treated 
in  their  homes  than  in  hospital.  As  the  graver  cases  and  the 
poorer  cases  tend  to  find  tlieir  way  to  hospital  and  as  the  act 
of  removal  is  often  undertaken  rather  late  in  the  disease  and 
is  not  always  beneficial  to  the  patient,  it  would  be  reason- 
able to  expect  a lower  mortality  among  patients  treated  at 
home.  A death-rate  in  the  neighbourhood  of  10  per  cent,  is 


2GS  THE  PROGNOSIS  AND  TREATMENT  OF 
suggested  by  general  practitioners  of  wide  experience.  The 
mortality  from  lobar  pneumonia  among  the  troops  at  Aider- 
shot  during  the  1914-18  War  was  shown  by  Abrahams  [2] 
to  be  as  low  as  10-5  per  cent.  Here  the  patients  were  mostly 
picked  men  of  military  age,  and  it  is  probable  that  they  were 
moved  to  hospital  in  the  earliest  stage  of  the  disease.  At  a 
base  hospital  in  France  Malloch  and  Ithea  [3]  found  a general 
mortality  of  2G-1  per  cent.,  with  a higher  rate  among  those 
coming  long  distances  by  convoy  or  hospital  train  than 
among  base  details.  Cecil  [4],  in  the  United  States,  re- 
ports that  the  death-rate  of  pneumococcal  pneumonia 
varies  considerably  with  the  class  of  patient  studied, 
being  lowest  in  private  practice,  somewhat  higher  in  the 
hospitals  of  the  better  class,  and  highest  in  the  large  hos- 
pitals draining  the  slum  areas.  Thus  the  mortality  at  the 
Rockefeller  Hospital  is  19-5  per  cent,  and  at  the  Bellevue 
Hospital  85-8  per  cent.  Among  422  cases  (all  types)  un- 
treated with  serum  Cecil  found  a mortality  of  nearly  30  per 
cent.  Among  429  cases  (all  types)  treated  with  serum  there 
was  a mortality  of  28  per  cent.  Even  this  lower  figure 
approaches  twice  the  Guy’s  Hospital  figure.  It  is  clear  that 
pneumonia  is  a more  serious  menace  in  the  United  States 
than  in  the  British  Isles. 

Turning  to  morbidity  in  hospital  cases  Waterfield  finds 
that  approximately  90  per  cent,  of  the  cases  which  recover 
do  so  without  disability,  so  that  there  is  no  overwhelming 
argument  in  favour  of  an  additional  therapy  on  this  score, 
even  though  it  be  shown  that  serum  is  capable  of  producing 
an  earlier  defervescence. 

Leaving  statistical  data,  let  us  next  consider  the  factors 
which  are  commonly  accepted  as  influencing  prognosis  in  the 
individual.  So  far  we  have  recognized  that  youth  and  good 
environment  are  favourable  and  that  poor  conditions  and 
advancing  years  are  unfavourable.  Other  prognostic  indi- 
cations have  been  repeatedly  observed  at  the  bed-side. 
The  presence  of  a chronic  disease  or  of  alcoholism  weights 
the  scales  against  recovery.  Cyanosis  is  adverse,  delirium 
by  no  means  necessarily  so.  Wide  extent  of  lung  involve- 
ment, although  frequently,  is  not  always  of  bad  import. 


LOBAR  PNEUMONIA  2(59 

A low  and  particularly  a falling  blood-pressure  gives  cause 
for  concern.  The  pulse-temperature-respirationratio  affords 
valuable  guidance ; while  parallelism  is  maintained  or  pulse- 
and  respiration-rate  are  slow  in  proportion  to  the  tempera- 
ture hopes  are  good,  but  if  pulse-  and  respiration-rate  rise 
unduly  while  the  temperature  swnngs  or  falls,  there  is  cause 
for  grave  anxiety.  A clean  tongue  and  nourishment  well 
taken  are  encouraging.  A good  leucocytic  response,  in  the 
neighbourhood  of  20,000  cells  per  c.mm.,  has  always  been 
accounted  favourable,  and  a complete  absence  of  leuco- 
eytosts  as  very  unfavourable.  Intermediate  figures  must  be 
balanced  with  the  clinical  findings.  The  pneumococcus  may 
be  grown  from  the  blood-stream  in  the  early  stages  of 
pneumonia  in  a certain  proportion  of  cases.  A profuse 
growth  or  persisting  positive  blood  cultures  as  the  disease 
advances  are  now  known  to  be  very  adverse.  Pericarditis 
and  meningitis,  other  expressions  of  the  septicaemic  state, 
usually  foretell  a fatal  termination.  Pneumococcal  peritoni- 
tis has  its  special  incidence  in  childhood  and  may  occur  with 
or  without  evident  pneumonia ; the  death-rate  is  high  but 
recoveries  occur. 

It  will  be  generally  agreed  that  prognosis  is  most  difficult 
during  the  first  three  days  of  the  disease — the  very  stage  in 
which  additional  help,  if  required,  should  be  given.  Nothing 
would  give  a greater  impetus  to  the  employment  of  serum 
therapy  than  the  establishment  of  prognostic  criteria  which 
would  separate  at  an  early  stage  the  15  or  20  per  cent,  of 
cases  with  an  otherwise  hopeless  prognosis  from  the  80  or 
85  per  cent,  destined  to  recover  spontaneously.  At  present 
reliance  must  be  placed  upon  clinical  judgement  of  the 
patient’s  constitution  and  reserves  and  of  the  extent  of  the 
infection  combined  with  a routine  leucocyte  count,  but  we 
must  acknowledge  that  appearances  can  be  deceptive.  11V 
have  all  seen  the  ‘apparently  hopeless’  case  recover,  and 
the  'apparently  favourable*  case  succumb. 

The  Essentials  of  Non-specific  Thekafy 

Although  it  cannot  be  quantitatively  expressed  it  is  not 
to  be  doubted  that  symptomatic  treatment  helps  recovery. 


270  THE  PROGNOSIS  AND  TREATMENT  OF 
and  that  good  or  bad  treatment  may  make  the  difference 
between  life  and  death.  A warm  but  fresh  and  well- 
ventilated  room  and  a good  nurse  are  probably  to  be  ac- 
counted of  greater  value  to  the  patient  than  all  other 
measures  combined.  The  nurse’s  mission  is  to  secure  the 
maximum  of  rest  and  sleep  with  the  minimum  of  inter- 
ference; to  supply  adequate  light  nourishment;  to  attend 
to  the  mouth  and  skin  without  unnecessary  movement  or 
fatigue ; to  limit  the  visits  of  relatives ; accurately  to  keep 
those  records  which  are  of  such  importance  to  the  physician 
as  indices  of  progress  or  deterioration;  to  preserve  op- 
timism; and  to  administer  oxygen  and  certain  drugs  nt 
appropriate  times.  A fussy  nurse,  too  insistent  on  profes- 
sional detail  or  appearances,  or  too  partial  to  heated  rooms 
and  the  pneumonia  jacket,  can  do  as  much  harm  as  her 
wiser  colleague  can  do  good.  While  most  patients  arc 
happier  propped  high  with  extra  pillows,  individual  re- 
quirements vary  and  the  elevation  can  be  overdone. 
Occasional  tepid  sponging  is  a part  of  the  routine.  A fluid 
or  semi-fluid  diet  with  fruit-juices  and  plentiful  drinks  and 
additional  sugar  or  glucose  is  usually  the  best.  Stimulants 
can  frequently  be  dispensed  with  altogether  if  adequate 
fluid  and  sugar  arc  taken,  or  alternatively  may  be  reserved 
for  the  anxious  days  before  the  crisis.  Hypodermic  stimu- 
lants such  as  strychnine  and  adrenaline  are,  to  my  mind,  of 
dubious  value.  They  are  often  given  rather  at  the  dictation 
of  anxiety  than  of  necessity,  and  if  they  produce  a physio- 
logical response  on  the  part  of  the  heart  or  blood-pressure 
is  it  not  rather  by  dint  of 1 Hogging  the  tired  horse’  and  too 
transitory’  in  its  effect  to  be  a real  boon  ? Digitalis  is  com- 
monly given  although  it  is  still  doubtful  whether  it  has  any 
virtue  in  the  case  of  a regular  tachycardia  and  embarrassed 
function  due  to  fever  and  toxaemia.  Brandy  is  a food 
ns  well  as  a stimulant  and  its  utility  in  certain  cases  and 
stages  is  generally  approved.  Oxygen,  preferably  given 
continuously  through  a nasal  catheter,  is  obviously  justified 
in  the  presence  of  cyanosis.  For  sleep,  when  pain  is  slight 
or  absent,  ^Dover’s  powder  with  aspirin  may  be  enough  for 
some  patients  and  in  small  doses  is  a useful  combination  in 


LOBAR  PNEUMONIA  271 

the  case  of  children.  Morphine  should  never  be  withheld 
during  the  earlier  stages  in  the  adult  case  wlieTe  sleepless- 
ness and  pain  are  prominent  complaints.  One  quarter  of 
a grain  should  be  the  dose,  a sixth  being  too  frequently 
disappointing  in  its  effect.  A light  flannel  jacket  or  shawl 
over  nightdress  or  pyjamas  is  sufficient  covering.  Heavy 
poultices,  thick  or  tightly  fitting  vests,  and  pneumonia 
jackets  are  to  be  avoided,  but  a light  linseed  or  antiphlogis- 
tin  poultice  is  grateful  in  the  presence  of  pleuritic  pain.  So 
far  as  is  consistent  with  careful  observation  the  patient 
should  be  spared  repeated  examinations  of  the  chest. 

Tiie  Method  and  Results  of  Serum  Therapy 

These  have  been  ably  summarized  by  Cecil  [4].  The 
method  is  based  upon  successful  protective  experiments 
with  artificially  infected  monkeys.  Felton’s  serum  has  the 
double  advantage  over  previous  preparations  of  being  con- 
centrated, so  that  smaller  quantities  can  be  given  at  a time, 
and  of  being  less  toxic.  The  procedure,  quoting  Cecil 
verbatim,  is  as  follows: 

‘The  patient  is  first  questioned  as  to  previous  injections  of  horse 
serum,  and  as  to  history  of  hay-fever,  asthma,  or  hives.  An  intrader- 
mal  and  a conjunctival  test  are  then  made  with  a 1 in  10  dilution  of 
normal  horse  serum.  If  after  15  minutes  these  tests  are  both  negative, 
5 c.cm.  of  Felton’s  serum  are  slowly  injected  intravenously.  If  the 
patient  shows  no  reaction  to  this  first  injection  of  serum,  a second  of 
15  to  20  c.cm.  is  given  intravenously  from  one  to  two  hours  later,  nnd 
this  dose  is  repeated  every  two  to  three  hours  until  the  patient  has 
received  approximately  100,000  units  (equivalent  usually  to  about 
100  c.cm.  serum).  The  amount  of  serum  administered  on  the  follow- 
ing day  is  determined  by  the  clinical  condition  of  the  patient.  If  his 
condition  has  improved  and  if  his  chart  shows  a decided  drop  in 
temperature,  pulse-rate,  and  respiration-rate,  the  amount  of  scrum 
administered  is  approximately  one-half  of  that  administered  on  the 
first  day.  If,  on  the  other  hand,  the  patient’s  condition  is  worse,  or  it 
it  remains  unchanged,  the  intensive  treatment  is  continued.  On  the 
third  day  the  same  policy  is  pursued.  If  the  patient’s  temperature 
la  under  100°  F.,  and  if  his  condition  is  good,  the  general  rule  ts  to 
give  one  or  possibly  two  10  c.em.  injections  to  prevent  relapse.  We 
haw  found  from  experience  that  if  any  benefit  is  to  result  from 
serum  treatment  it  is  usually  apparent  oftcr  two  or  at  least  three 
days  of  treatment.* 


272  THE  PROGNOSIS  AND  TREATMENT  OF 

The  difficulties  and  anxiety  attending  such  a programme  . 
outside  hospital  require  no  emphasis.  Even  spacing  out 
the  injections  to  eight  hours  and  giving  larger  quantities 
does  not  greatly  simplify,  and  serum  reactions,  which  are 
a genuine  cause  of  apprehension,  have  not  been  wholly 
eliminated. 

Treating  alternate  cases  without  preliminary  typing, 
Cecil  obtained  a reduction  of  mortality  from  36  per  cent, 
to  28  per  cent,  in  groups  of  cases  numbering  respectively 
422  and  429.  A reduction  in  the  same  ratio  (provided  all 
cases  were  seen  early  enough  and  considered  suitable  for 
serum)  would  convert  the  16  per  cent.  Guy’s  Hospital 
mortality  to  12  per  cent.,  and  the  private  practice  10  per 
cent.,  say,  to  8 per  cent. 

Approximately  two-thirds  of  all  cases  of  lobar  pneumonia 
are  due  to  Types  I and  II,  and  approximately  one-third 
are  due  to  Type  I infections.  The  mortality  in  Type  I 
cases  has  been  reduced  from  81*2  to  20*1  (Cecil)  and  from 
30-9  to  16*6  per  cent,  (combined  results  of  various  investi- 
gators quoted  by  Cecil).  In  Type  II — the  most  virulent 
type — the  results  are  less  good,  a reduction  from  45-8  to 
40-5  per  cent,  only  being  reported  (Cecil),  and  from  37-7  to 
24- G per  cent,  (other  investigators  quoted  by  Cecil).  The 
earlier  treatment  is  instituted  the  better  are  the  results. 
Cecil  reports  a reduction  in  mortality  from  26*8  to  11*7  per 
cent,  in  Type  I cases  treated  within  72  hours  of  onset.  I 
have  seen  no  figures  thus  far  which  suggest  that  the  inci- 
dence of  complications  such  os  empyema  is  influenced  by 
serum  therapy.  Armstrong  and  Johnson  [5]  also  state  that 
complications  and  sequelae  are  apparently  uninfluenced  by 
serum.  The  results  obtained  by  the  Scottish  [Gj  and  English 
[5]  investigators,  although  their  studies  so  far  have  been  on 
a smaller  scale,  support  the  contentions  of  Cecil.  AH  ob- 
servers are  agreed  that  there  is  an  appreciable  reduction  in 
mortality  and  that  early  defervescence  is  more  frequent 
among  cases  treated  with  serum.  Similar  claims,  it  is  true, 
have  previously  been  made  on  behalf  of  vaccine  treatment 
and  certain  forms  of  drug  therapy,  but  no  such  carefully 
controlled  studies  have  been  reported  by  their  advocates. 


LOBAR  PNEUMONIA  278 

An  unexpectedly  early  defervescence  may  also  occur  with- 
out specific  therapy,  but  not  with  the  frequency  observed 
in  serum-treated  cases.  Finally,  there  is  evidence  for  the 
specificity  of  Felton’s  serum  in  that  the  mortality  of  Type 
III  and  Type  IV  infections  is  not  appreciably  influenced 
by  it.  In  other  words,  improvement  depends  upon  some- 
thing more  than  a ‘protein-shock’  effect.  Criticisms  of  the 
methods  of  control  employed  in  the  reported  series  could 
easily  be  advanced,  for  adequate  controls  in  large-scale 
human  experiments  of  this  kind  are  difficult  to  come  by. 
Thus  in  the  ‘alternate-case’  method  it  is  clear  that  an 
accidental  preponderance  of  cases  of  more  favourable  age 
and  constitution  in  the  treated  group  would  lower  the 
mortality  appreciably.  However,  the  factors  influencing 
the  liability  to  death  or  recovery  in  pneumonia  are  so 
numerous  that  precise  analysis  is  impossible,  and  when 
various  groups  of  reliable  workers  find  essential  agreement 
their  opinions  must  be  held  worthy  of  acceptance. 

Practical  Difficulties  of  Serum  Treatment 

(1)  These  are  firstly  encountered  in  connexion  with 
diagnosis,  and  particularly  with  diagnosis  at  a suitably 
early  date.  The  doctor  is  not  always  called  at  the  onset  of 
the  disease  and  two  or  three  days  must  frequently  elapse 
before  he  appears  on  the  scene  or  before  the  diagnosis  is 
certain.  Typing  requires  a further  twelve  to  twenty-four 
hours,  even  if  a competent  laboratory  service  be  close  at 
hand.  Not  all  lobar  pneumonias  are  pneumococcal  and, 
although  an  abrupt  onset,  high  fever,  and  rusty  sputum  are 
generally  accurate  tale-bearers,  there  are  cases  in  which  the 
differentiation  of  a pneumococcal  from  an  ‘influenzal*  or 
streptococcal  pneumonia  ora  ‘mixed’  broncho-pneumonia 
is  none  too  easy.  In  recent  years  other  types  of  pneumonia 
have  been  more  common  and  pneumococcal  pneumonia  less 
common  than  formerly.  Massive  collapse  in  association  with 
bronchitis,  a comparatively  benign  condition,  may  also  be 
mistaken  for  pneumonia. 

(2)  Even  allowing  that  an  early  diagnosis  is  achieved 

T 


274  THE  PROGNOSIS  AND  TREATMENT  OF 
and  the  case  thought  suitable  for  serum,  the  necessary 
preliminaries  and  the  frequent  administrations  of  serum 
by  the  intravenous  route  must  needs  provide  the  busy 
practitioner  with  very  real  embarrassment.  They  may  also 
be  disturbing,  both  physically  and  mentally,  to  patients  for 
whom  we  normally  advocate  the  minimum  of  disturbance. 

(0)  In  the  case  of  a poor  patient  it  must  be  decided 
whether  to  rely  upon  conservative  treatment  at  home  or  to 
risk  removal  to  a hospital  where  serum  treatment  can  be 
instituted  if  the  infection  prove  to  be  of  appropriate  type. 

While  grateful  for  new  knowledge  we  must  confess  that 
it  can  greatly  complicate  judgement  and  practice.  We 
would  none  of  us  willingly  withhold  a curative  agent  in  an 
anxious  disease,  but  while  we  know  that  there  is,  broadly 
speaking,  a 4 to  1 prospect  of  spontaneous  recovery  and  a 
1 in  3 chance  that  the  infection  is  of  inappropriate  type, 
we  may  feel  a pardonable  disinclination  to  burden  a patient 
with  repeated  doses  of  an  intravenous  remedy  for  an  inde- 
terminate advantage.  On  the  other  hand,  we  cannot  put 
it  from  our  minds  that  a certain  small  percentage  of  other- 
wise doomed  cases  may  have  the  balance  tipped  in  their 
favour  by  serum. 

As  an  example  of  the  judicial  difficulties  which  may  be 
encountered  let  me  quote  the  case  of  a friend  and  colleague 
to  whom  I was  called  the  day  after  hearing  the  arguments 
in  favour  of  serum  therapy  set  forth  by  its  chief  exponents. 

patient’s  age  was  C3;  bis  life  had  been  healthy  end  hard- 
working. On  23  July  he  felt  chilly  and  unwell.  The  next  day  he 
remained  at  work  still  feeling  unfit.  On  the  25th  he  felt  well  again. 
On  the  2Gth  he  had  a rigor  while  out  in  his  car,  and  that  night  his 
temperature  was  102°.  I saw  him  on  the  evening  of  the  2Sth — i.e.  the 
second  day  from  the  rigor  and  the  fifth  from  his  first  symptoms  of 
infection — and  found  signs  of  pneumonia  at  the  right  apex  and  at 
the  right  root  behind.  Respirations  30.  Pulse  108.  General  condition 
good.  Leucocyte  count  25,000  cells  per  c.mm.  A small  specimen  of 
rusty  sputum  was  obtained.  An  attempt  to  type  the  pneumococcus 
by  Armstrong's  [7]  direct  method  was  unsuccessful,  but  the  next 
morning  it  was  reported  as  Type  I. 

On  29  July  there  was  considerable  restlessness  with  delirium,  and 
enough  cyanosis  to  justify  continuous  oxygen  at  night.  On  the  30th 
the  left  upper  and  lower  lobes  became  involved.  On  the  31st  he  looked 


LOBAR  PNEUMONIA  275 

distinctly  worse.  Respirations  30-6.  Pulse  130,  with  frequent  inter- 
missions.  Breathing  was  embarrassed  by  meteorism,  which  was 
relieved  by  pituitrin  and  a turpentine  enema.  There  was  also  severe 
pleuritic  pain  below  the  left  nipple.  By  2 August  (the  seventli  day 
after  the  rigor)  the  temperature  had  fallen  to  99  0°,  the  respirations 
to  24,  and  the  pulse-rate  to  92.  After  steady  improvement  for  a 
fortnight  he  began  to  get  up,  but  then  developed  a dry  pleurisy  first 
at  the  right  and  then  at  the  left  base  without  any  serious  rise  in 
temperature,  and  with  a leucocyte  count  of  only  9,000.  The  pleurisy 
took  some  weeks  to  clear,  but  the  case  gave  us  no  further  anxiety. 

Here  were  some  of  the  difficulties.  Should  I regard  the  day 
on  which  the  typing  was  complete  as  the  third  or  the  sixth 
day  of  infection  ? Accepting  it  as  the  third  day,  should  I be 
influenced  by  the  patient’s  age  and  the  knowledge  that  he 
had  a Type  I infection  and  give  him  serum  ? Or  knowing 
him  to  be  abstemious  and  of  sound  constitution,  and  com- 
forted by  the  good  leucocytosis,  should  I rely  on  the  old 
expectant  measures  ? I chose  the  latter  course,  not  without 
heart  searchings,  but  in  the  event  justifiably.  In  two  other 
cases  which  ended  fatally  I have  criticized  myself  afterwards 
for  withholding  serum,  although  at  the  time  I had  reasons 
for  my  conservatism.  From  more  recent  evidence  it  would 
appear  that  the  mortality  after  the  age  of  50  is  little,  if  at 
all,  influenced  by  serum. 

Conclusions 

It  remains  to  attempt  advice  in  practical  form.  At 
present  no  unalterable  rules  can  be  laid  down  with  regard 
to  the  indications  for  serum  in  lobar  pneumonia.  As  in  all 
therapeutic  decisions  the  final  plan  must  be  based  upon  the 
particular  state  and  requirements  of  the  individual  patient. 
The  method  is  clearly,  and  (unless  it  can  be  simplified) 
must  remain,  more  suited  to  hospital  than  home  conditions. 
It  is  contra-indicated  in  children  and  adolescents  for  the 
most  part,  since  the  natural  recovery-rate  is  so  high  in  this 
age-period.  It  may  reasonably  be  decided  to  dispense  with 
it  in  advanced  age  when  interference  is  ill-tolerated,  and 
the  disease  frequently  provides  a blessed  escape  from 
infirmities.  I should  personally  hesitate  to  employ  it  in  any 
subject  with  known  allergic  tendencies,  for  I am  doubtful 


276  THE  PROGNOSIS  AND  TREATS  IENT  OF 
whether  the  ill  effects  of  serum  shock  at  the  beginning  or  of 
serum  sickness  at  the  end  of  a pneumonia  would  be  propor- 
tionately counterbalanced  by  the  benefits  of  the  treatment. 
In  previously  healthy  adults  showing  a good  initial  response 
to  infection  and  a high  Ieucocytosis,  I should  feel  justified 
in  withholding  serum.  We  are  thus  left  -with  adult  cases 
giving  cause  for  undue  anxiety  at  an  early  stage  and  showing 
a failure  of  Ieucocytosis;  alcoholics  might  be  included  in 
this  group.  To  these  it  should  be  justifiable  to  give  an  early 
dose  of  Felton’s  serum,  and  to  continue  the  treatment  if 
the  organism  is  found  to  be  of  appropriate  type.  The  treat- 
ment is  more  worthy  of  consideration  in  Type  I than  in 
Type  II  infections.  At  present  these  restrictions  would 
seem  to  me  reasonable  in  institutions  where  costs  must 
be  carefully  counted,  and  in  private  practice.  Expense 
prohibits  the  treatment  of  poor  patients  in  their  homes.  In 
such  cases  the  difficult  decision  of  whether  or  not  to  counsel 
removal  to  hospital  must  be  made.  If  the  disease  has 
reached  its  third  day  and  adequate  nursing  and  attention 
can  be  secured,  I should  usually  prefer  to  keep  the  patient 
at  home  and  to  forgo  the  possible  advantages  of  laboratory 
study  and  serum  therapy.  Removal,  if  necessary’,  should 
be  carried  out  within  the  first  48  hours. 

While  the  employment  of  serum  in  pneumonia  on  a wide 
scale  cannot  be  advocated,  its  claims  cannot  be  overlooked. 
It  is  furthermore  possible  that  a collective  investigation  of 
prognosis  and  a more  critical  search  for  special  indications 
may  serve  to  lighten  the  physician’s  burden  of  decision,  to 
simplify  his  task,  and  to  reduce  a little  further  the  compara- 
tively low  death-rate  from  pneumococcus  Types  I and  II 
which  obtains  in  this  country  among  previously  healthy 
persons.  Of  our  15-20  per  cent,  of  deaths,  be  it  remembered, 
a certain  proportion  occur  among  ‘bad  lives’  which  are 
unlikely  to  be  reclaimed  by  any  treatment.  Others  again 
are  due  to  infective  strains  against  which  we  have  as  yet 
no  potent  serum.  With  a suitable  card  system  observers 
in  general  practice  might,  I believe,  greatly  assist  a collec- 
tive inquiry  into  the  matter  of  prognosis.  It  is  to  be  hoped 
that  hospital  and  laboratory  workers  will  continue  their 


LOBAR  PNEUMONIA  277 

studies  of  method  and  indications,  and  that  the  firms 
responsible  for  the  supply  of  serum  will  find  it  possible  to 
reduce  the  costs. 


REFERENCES 

1.  Ryle,  J.  A.,  and  Water  field,  R.  L.:  Guy's  Ilosp.  Reports,  1033, 

Jxxxiii.  389. 

2.  Abrahams,  A.:  Lancet,  1020,  ii.  543. 

3.  Maxxoch,  A.,  and  Riiea,  L.  J.:  Joum.  Royal  Army  Med.  Corps, 

1918,  xxxi.  300. 

4.  Cecil,  R.  L.r  Brit.  Med.  Joum.,  1032,  ii.  657. 

5.  Armstrong,  R.  R.,  and  Joitnson,  R.  S.:  ibid.,  p.  602. 

G.  Physicians  to  the  Royal  Infirmary,  Edinburgh:  Lancet,  1030, 
ii.  1890 ; and  Physicians  to  the  Royal  Infirmary,  Glasgow:  ibid., 
p.  1387. 

7.  Armstrong,  R.  R.:  Brit . Med.  Joum.,  1932,  i.  187. 

This  chapter  has  been  left  as  it  originally  stood  in  illustration  of  the 
state  of  knowledge  regarding  prognosis  in  lobar  pneumonia  and  the 
effects  of  treatment  on  it  prior  to  the  introduction  of  the  sulphonamfdes 
and  penicillin.  We  still  require  more  precise  knowledge  of  the  special 
indications  at  different  age-periods.  It  is  not  always  kind  to  reclaim 
the  very  elderly  with  potent  remedies  which  may  check  their  lung 
disease  but  fail  to  give  them  back  their  faculties  and  enjoyment  of 
living.  The  actual  mortality  for  the  several  age-groups  and  the  differ- 
ent socio-economic  groups  and  in  types  of  pneumonia  not  due  to  the 
pneumococcus  have  also  to  be  better  determined  for  countries,  races, 
and  communities  and  in  separate  epidemic  periods.  Without  them 
therapeutic  assessments  will  remain  incomplete  and  less  reliable  than 
they  might  he. 


XX 

PROGNOSIS 

The  three  main  tasks  of  the  clinician,  be  he  physician, 
surgeon,  or  specialist,  are  diagnosis,  prognosis,  and  treat- 
ment. Of  these  diagnosis  is  by  far  the  most  important,  for 
upon  it  the  success  of  the  other  two  depends.  It  is,  however, 
•with  prognosis  as  a part  and  product  of  clinical  discipline 
that  this  chapter  is  concerned.  In  my  recollection  it  has 
been  a common  grumble  among  students  that  ward  teaching, 
as  a whole,  is  over-insistent  on  diagnosis  and  allows  too  little 
time  for  therapeutic  discussion.  I remember  no  such  refer- 
ence to  the  neglect  of  prognosis  in  bedside  teaching.  At 
that  stage,  perhaps,  the  student  has  scarcely  come  to  a full 
recognition  of  its  importance.  And  yet,  difficult  though 
it  be,  instruction  in  prognosis  should  surely  be  given  far 
more  consideration  than  it  commonly  receives.  It  should 
anticipate  treatment  in  the  discussion  at  the  bedside — or, 
preferably,  at  a discreet  distance  from  it.  Diagnosis  is  really 
incomplete  and  sound  treatment  and  the  assessment  of  the 
results  of  treatment  are  impossible  without  that  rational 
forecasting  based  on  pathology,  statistics,  and  observational 
experience  which  we  call  prognosis.  Prognosis  requires  a 
better  appreciation  of  the  whole  pathology  of  a case  or  a 
disease  than  present  diagnosis,  and  although  the  future  con- 
tains even  more  variables  and  unknowns  than  the  recent 
past,  it  is  none  the  less  possible  to  establish  guiding  principles 
in  prognosis  which  improve  method  and  bring  advantage  to 
the  patient  and  his  doctor  and,  in  many  conditions,  allow  a 
high  degree  of  accuracy.  Prognosis  is  essentially  a physi- 
cianly  task.  The  pathologist,  the  biochemist,  and  the  radio- 
logist, although  they  may  greatly  assist  that  task,  have  no 
immediate  concern  with  it . The  study  of  prognosis  is  some- 
times considered  academic  rather  than  practical,  but  this 
is  a narrow  and  unwarranted  view.  For  the  sake  of  our 
patients  and  their  relatives  and  for  the  ordering  of  our  judge- 
ments it  is  a daily  duty ; for  the  improvement  of  our  under- 


PROGNOSIS  279 

standing  of  pathological  processes  and  to  help  us  to  see 
them  in  their  true  perspective  it  is  an  essential  discipline. 

The  Meaning  and  Uses  of  Prognosis 

Hippocrates  said:  ‘I  hold  that  it  is  an  excellent  thing  for 
the  physician  to  practise  forecasting.  For  if  he  discover  and 
declare  unaided  by  the  side  of  his  patients  the  present,  the 
past  and  the  future,  and  fill  in  the  gaps  in  the  account  given 
by  the  sick,  he  -will  be  the  more  believed  to  understand  the 
cases,  so  that  men  will  confidently  entrust  themselves  to 
him  for  treatment.  Furthermore,  he  will  carry  out  the 
treatment  best  if  he  know  beforehand  from  the  present 
symptoms  what  will  take  place  later.’ 

These  views  and  the  famous  prognostic  aphorisms  were 
based  on  clinical  experience  alone,  with  none  of  the  checks 
or  confirmations  furnished  by  pathology  or  by  biochemical 
or  other  modem  assessments  of  degrees  of  tissue  damage  or 
functional  impairment.  In  this  regard  they  may  appear  the 
more  remarkable,  but  we  should  also  remember  that,  lacking 
scientific  aids  and  specific  remedies,  Hippocrates  was,  in 
fact,  compelled  to  train  his  mind  and  form  his  judgements  on 
the  basis  of  an  undistracted  study  of  the  natural  course  and 
history  of  the  diseases  which  came  to  his  notice.  In  other 
words,  he  employed  methods  appropriate  to  what  would 
now  be  called  the  F ollow-up  Clinic,  of  which  he  may,  perhaps, 
be  acclaimed  the  first  founder. 

An  understanding  of  the  natural  or  undisturbed  course  of 
a disease  must  provide  the  basis  of  all  prognostic  assess- 
ments. In  many  conditions  to-day  this  course  can  be  greatly 
modified  by  specific  treatments,  by  surgery,  or  by  altered 
modes  of  life.  In  other  conditions  our  endeavours  still  have 
little  influence.  In  others  again  unwise  interference  may,  and 
too  often  does,  give  an  adverse  bias  to  the  patient’s  prospects. 
Advancing  knowledge  has  both  assisted  and  complicated 
prognosis.  The  assistance  has  come  through  new  diagnostic 
methods  and  tests  of  function  and  the  provision  of  specific 
remedies;  the  complication  through  the  influence  of  new 
and  potent,  but  sometimes  more  hazardous  treatments,  or 
the  multiplication  of  alternative  treatments.  To  take  an 


280  PROGNOSIS 

example,  we  now  have  more  precise  methods  of  assessing 
degrees  of  thyrotoxicosis.  By  means  of  improved  assess- 
ments we  have  to  decide  between  medical  treatment,  X-ray 
treatment,  and  operation  in  the  individual  case.  Either  the 
withholding  or  the  employment  of  a particular  measure  may 
entail  risks  to  health  or  sometimes  even  to  life. 

Prognosis  is  often  held  to  imply  no  more  than  a decision 
as  to  whether  the  patient  will  recover  or  not,  or  an  estimate 
of  the  duration  of  his  disease.  Just  as  diagnosis  means 
‘through’  (or  thorough)  knowledge  of  a case  and  is  some- 
thing more  than  mere  nomenclature  or  a label,  so,  too, 
prognosis  (or  foreknowledge)  should  mean  a visualization 
and  reasoned  presentation  of  all  the  events  which  ore  likely 
to  mark  the  future  course  of  a particular  disease  affecting  a 
particular  patient,  and  not  a mere  forecast  of  duration  and 
outcome.  Nevertheless,  judgement  in  practice  must  clearly 
be  guided  by  mortality  statistics  and  a knowledge  of  the 
prognosis  of  diseases  as  a whole,  be  they  dangerous  or  trivial. 

Prognosis  as  a Durr 

In  what  respects  is  prognosis  to  be  regarded  as  a duty, 
that  is  to  say  as  a normal  and  proper  physicianly  function  ? 
In  all  serious  illnesses,  in  many  less  serious  conditions,  and 
in  some  which  are  trivial  in  the  doctor’s  eyes,  but  neverthe- 
less a cause  of  anxiety  to  the  patient,  the  main  interest  of 
the  patient  and  his  relatives  (apart  from  the  immediate 
relief  of  symptoms)  is  to  know  what  the  issue  of  the  illness 
will  be  rather  than  its  precise  nomenclature.  They  do,  in 
point  of  fact,  want  to  know  the  diagnosis,  but  solely  or 
chiefly  as  a guide  to  prognosis.  A troublesome  cough  or  an 
abdominal  pain  is  apt  to  imply  pulmonary  tuberculosis 
or  appendicitis  or  cancer  to  the  lay  mind  until  assurance  is 
given  to  the  contrary.  Comfort  and  reassurance,  indeed, 
play  a part  in  treatment  which,  although  their  influence 
cannot  be  measured,  are  universally  accepted  as  essential 
contributions  to  progress  and  even  to  recovery.  In  organic 
as  well  os  functional  diseases  we  are  becoming  steadily  more 
Impressed  by  the  inter-relationships  of  emotion  and  bodily 
change.  Anxiety  is  the  most  prevalent  of  all  the  harmful 


PROGNOSIS  281 

emotions.  The  best  counter  to  anxiety  is  a good  prognosis.  It 
is  not  without  significance  that  the  ablest  and  most  success- 
ful physicians  have  also  included  among  their  number  the 
most  optimistic.  A change  in  the  whole  feeling  and  attitude 
of  a patient  and  his  or  her  relatives  not  infrequently  dates 
from  the  visit  of  a family  doctor  or  consultant  who  has  been 
at  pains  to  emphasize  the  likelihood  of  a good  recovery.  I 
find  it  difficult  to  credit  that  there  exist  doctors  who  tell 
their  patients — save  in  exceptional  circumstances — that 
their  condition  is  hopeless,  and  yet  in  taking  histories  how 
often  one  has  been  told  that  ‘my  doctor  said  I could  not 
recover*,  or  ‘they  only  gave  me  a week  to  live*,  or  ‘three 
doctors  gave  me  up  Let  us  admit  that  patients,  like  all  of  us, 
are  apt  to  exaggerate  dramatic  or  adventurous  experience, 
and  that  usually  these  gloomy  prognostications  must  have 
reached  them  at  a later  date ; even  so  it  is  clear  that  the 
relatives  must  have  had  to  submit  to  an  unnecessarily  sad 
and  head-shaking  interview.  Such  pessimism,  and  this  is 
the  point  I would  make,  is  repeatedly  proved  unjustifiable 
by  the  event.  Doctors,  in  other  words  (although  their  good 
prognoses  are  more  rarely  wrong),  repeatedly  fall  short  in 
their  prognostic  judgements.  Need  they  fail  so  often  and 
need  their  bias  so  frequently  be  adverse?  Excepting  in 
inoperable  cancer,  until  lately  bacterial  endocarditis,  a few 
other  rare  progressive  maladies,  and  obviously  moribund 
states,  we  have  no  such  certainty  of  a fatal  result  as  some 
of  us  are  apt  to  assume.  The  longer  we  live  the  more  lessons 
we  receive  in  respect  of  the  remarkable  recoverability  of  the 
human  body  from  grave  diseases,  from  pneumonias  and 
septicaemias,  from  heart-failures  and  grave  haemorrhages 
and  accidents.  Very  few  of  the  common  acute  diseases  have 
an  over-all  mortality  even  approximating  to  50  per  cent. 
Excepting  at  the  extremes  of  life  and  in  a small  group  of 
diseases  at  present  unconquerable  the  chances  of  recovery 
are  generally  greater  than  those  of  demise.  Children  especially 
have  great  recuperative  powers. 

It  is  therefore  wise  and  just  to  make  a point  of  giving  a 
good  prognosis  (whether  the  patient  has  questioned  it  or  not) 
in  all  cases  in  which  the  clinical  evidence  and  pathological 


2S2  PROGNOSIS 

knowledge  allow  it,  and  where  doubt  exists  at  least  to  give 
the  patient  the  benefit  of  the  doubt.  In  cases  where  the 
doctor  himself  is  anxious  and  uncertain  it  is  still  reasonable 
and  kindly  and  useful  to  stress  the  favourable  points  in 
discussing  the  case  with  relatives  and,  ns  for  the  patient,  to 
congratulate  him  on  his  gains,  his  courage,  and  his  co-opera- 
tion while  excluding  adverse  auguries  from  the  conversa- 
tion. In  the  process  of  assembling  ‘pros’  and  ‘cons’  for 
the  communicated  opinion,  the  considered  prognosis  takes 
better  shape;  the  partial  expressed  opinion,  in  fact,  assists 
the  whole  reserved  opinion.  Sir  Alfred  Fripp  used  to  say  to  his 
students,  ‘If  we  cannot  be  clever  we  can  always  be  kind’. 
With  experience  and  the  years  to  help  us,  we  need  not 
despair  of  educating  both  qualities.  In  states  of  ill  health 
due  to  anxiety,  and  especially  in  those  due  wholly  or  partly 
to  the  fear  of  disease,  a good  prognosis  is  almost  the  whole 
of  treatment  and  frequently  achieves  a cure. 

Just  as  a good  prognosis  is  calculated  to  do  good,  so,  too, 
a bad  one  may  do  an  infinity  of  harm  and  cast  a cloud  of 
gloom  upon  a household  which  will  with  difficulty  be 
prevented  from  finding  its  way  into  the  sick-room.  Some 
men  through  native  caution  or  a fear  of  loss  of  reputation 
decline  to  say  openly  that  a patient  may  get  well  when  it 
seems  possible  that  he  may  die.  To  give  no  prognosis  is 
almost  as  culpable  as  to  give  a bad  one  and  is  an  evasion  of 
responsibility.  It  is  always  possible  to  give  what  is  called  a 
‘guarded  prognosis’.  Wrongly  placed  optimism,  provided 
it  is  not  careless  or  breezy  or  accompanied  by  a disregard 
for  sensibilities  or  a neglect  of  therapeutic  detail,  will  rarely 
be  held  against  a doctor.  Wrongly  placed  pessimism,  on  the 
other  hand,  will  always  be  held  against  him  and  even 
pessimism  justified  by  events  quite  frequently  so. 

You  may  say  that  this  policy  of  the  reassuring  prognosis 
is  not  compatible  with  intellectual  honesty.  I beh'eve  it  to 
be  perfectly  compatible,  so  longas  we  do  not  delude  ourselves. 
As  scientists  we  do  not  bow  to  the  foolish  and  impossible 
request  of  the  law  to  tell  the  whole  truth  and  nothing  but 
the  truth.  We  discover  as  much  of  it  as  we  can,  but  remem- 
bering the  limits  of  our  precision  we  should  recognize  that 


PROGNOSIS  283 

it  would  be  as  unjust,  through  fear  of  error,  to  withhold 
comment  on  the  more  favourable  features  of  a case,  however 
few  they  be,  as  it  would  be  to  withhold  any  other  helpful 
measure  of  treatment.  If  or  when  the  outlook  becomes 
absolutely  bad,  then  we  must  impart  our  view  to  the  relatives. 
Before  that  it  is  no  failure  of  duty  or  honesty  of  purpose — 
while  the  mind  is  taking  counsel  with  itself — to  give  rather 
more  hope  than  the  moment’s  uncertainty  may  seem  to 
justify. 

It  is  very  important  at  times  for  the  patient  or  relative  to 
know  how  long  an  illness  will  last.  If  the  illness  be  pneumonia 
or  a duodenal  ulcer  or  a Pott’s  fracture  we  can  give  a fairly 
close  estimate  both  in  regard  to  the  bedridden  and  the 
convalescent  phases  of  treatment.  In  other  conditions  we 
may  only  be  able  to  give  a very  rough  estimate,  but  for 
economic  and  other  reasons  even  this  is  greatly  appreciated. 

Prognosis  is  a duty  in  another  important  sense  in  that  it 
must  constantly  guide  our  treatment.  To  this  end  we  must 
formulateourjudgementswiththegreatestaccuracypossible, 
assessing  the  probable  course  of  the  disease,  learning  (in 
order  to  foresee)  complicationswhichmaydcmandalterations 
in  treatment;  visualizing,  in  short,  a total  or  consecutive 
rather  than  an  immediate  pathology.  We  should  also  train 
ourselves  to  observe  the  strictest  impartiality  in  assessing 
the  proportionate  contributions  of  time  and  nature  on  the 
one  hand  and  of  our  own  ministrations  on  the  other.  To 
accomplish  all  this  we  must  needs  be  as  diligent  in  our 
search  for  prognostic  as  for  diagnostic  signs. 

Before  leaving  this  aspect  of  the  subject  let  me  relate  a 
single  case  in  which  the  outlook  seemed  desperately  bad, 
but  in  which  a grave  prognosis  proved  to  be  quite  unjustified. 
Any  physician  or  surgeon  of  experience  will  have  seen  other 
cases  in  plenty  which  seemed  as  desperate  but  in  which 
recovery  followed. 

Case  1.  Many  years  ago  I was  called  in  consultation  to  the  ease  of  a 
young  woman  in  the  sixth  month  of  pregnancy  who  had  fallen  victim 
to  a very  severe  attack  of  anterior  poliomyelitis,  sustaining  a flaccid 
paralysis  of  all  four  limbs  and  many  trunk  muscles.  As  there  was  no 
early  improvement  and  as  the  possibility  of  her  going  through  the  later 


281  PROGNOSIS 

weeks  of  pregnancy  and  parturition  seemed  out  of  the  question,  an 
attempt  was  made  to  induce  labour.  This  failed,  and  a Caesarean 
section  was  performed.  A few  days  later  she  developed  acute  intes- 
tinal obstruction  from  an  adhesion  between  the  small  bowel  and  the 
uterine  scar.  With  extensive  paralysis  in  numerous  muscle  groups, 
profound  exhaustion,  persistent  tachycardia,  and  some  respiratory 
embarrassment,  her  condition  seemed  desperate  and  her  hopes  of 
happy  and  active  life  remote  even  should  she  survive  another  opera- 
tion. Several  colleagues  met  in  consultation.  At  first  I argued  that 
it  might  be  kinder  to  give  morphine  and  interfere  no  more.  An  older 
and  a wiser  physician  took  the  view  that  we  should  still  seek  to  save 
life  and  that  wc  could  not  forecast  the  degree  of  recoverability  of  her 
paralysed  muscles.  A Paul’s  tube  was  inserted  and  she  recovered 
from  the  emergency.  But  she  did  more,  for  gradually,  after  months  of 
weary  waiting  and  devoted  care,  she  made  an  almost  complete 
recovery  from  all  her  disabilities  and  was  able  to  walk  and  dance  and 
lead  a happy,  active  life  again. 

I have  never  been  a pessimist.  From  this  case  I learned 
two  valuable  lessons : (1)  that  there  were  even  fewer  occasions 
than  I had  supposed  for  absolute  pessimism,  and  (2)  that  the 
most  extensive  cases  of  poliomyelitis  sometimes  make  the 
most  complete  recoveries.  Had  the  case  been  one  of  intestinal 
obstruction  from  an  inoperable  and  painful  growth  in  an 
old,  enfeebled  person,  the  judgement  might  obviously  have 
been  a very  different  one,  for  the  ultimate  issue  and  the 
intervening  misery,  despite  a temporary  relief  of  the  obstruc- 
tion, would  have  been  disputed  by  none. 

Phognosis  as  a Discipline 

There  is  always  a pleasant  sense  of  satisfaction  in  the 
achievement  of  a correct  diagnosis.  It  is  just  a little  too  easy 
to  rest  on  the  laurels  of  that  achievement.  As  I have  else- 
where insisted,  diagnosis  should  strictly  mean  the  thorough 
knowledge  of  a case.  It  involves  not  merely  a correct  label, 
but  an  understanding  of  the  patient,  a familiarity  with  his 
environment  and  with  the  antecedents  of  his  malady,  an 
appreciation  of  his  inherited  constitution  and  his  psycho- 
logical type,  together  with  a proper  appraisement  of  symp- 
toms, signs,  and  accessory  findings.  It  requires  a working 
knowledge  of  morbid  anatomy,  physiology,  and  psychology. 
Prognosis  requires  all  these  and  more.  It  requires  acquain- 


PROGNOSIS  285 

tance  with  mortality  and  morbidity  statistics,  with  the 
death  rate  in  different  age  periods,  with  the  constitutional 
factors  which  increase  or  lessen  morbidity,  with  the  good 
and  bad  effects  in  differing  circumstances  of  certain  treat- 
ments, with  the  signs  and  symptoms  not  merely  of  the  disease 
but  of  a good  or  bad  response  to  the  disease.  Prognostic 
ability,  in  brief,  is  bom  largely  of  pathology  and  patiently 
gathered  clinical  experience.  It  evolves  even  more  slowly 
than  diagnostic  ability.  Minute  and  careful  clinical  observa- 
tion, a good  visual  memory,  and  that  necessary  inquisitive- 
ness about  the  subsequent  course  of  cases  which  is  nowadays 
systematized  in  the  follow-up  inquiry  may  all  be  numbered 
among  the  handmaidens  of  prognosis. 

Prognosis  might  almost  be  defined  as  the  continuous  study 
of  living  pathology  and  in  this,  although  it  is  often  accounted 
an  art,  I would  submit  that  it  can  become  a scientific  process. 
We  are  sometimes  too  content  with  a static  pathology,  but 
a biological  process,  whether  physiological  or  pathological, 
is  never  static.  Inflammation  spreads  or  recedes,  bleeding 
is  arrested  or  continues,  destruction  and  degeneration 
advance  or  are  succeeded  by  repair.  Whether  through 
clinical,  pathological,  statistical,  or  other  methods,  we 
should  bend  our  best  endeavours  to  making  prognosis  more 
scientific.  Science  is  not  only  that  which  is  deemed  exact. 
The  science  of  meteorology  is  partly  concerned  with  pro- 
gnosis and  bases  its  forecasting  on  scientific  observations. 
Like  medicine,  its  prognoses  are  baffled  by  unknowns  and 
variables.  Whether  they  will  ever  attain  such  a degree  of 
accuracy  as  medical  prognosis,  for  all  its  shortcomings,  has 
already  attained  I cannot  say.  Weather  forecasts  can  concern 
themselves  with  short-term  judgements  only.  Medicine  has 
a constant  interest  and  a considerable  tale  of  achievement 
both  in  immediate  and  remote  prognosis. 

Strictly  speaking,  the  physician  should  ask  himself  in 
every  ease:  (1)  What  is  the  immediate  prognosis?  (2)  What 
is  the  remote  prognosis  ? (3)  What  are  the  possible  complica- 
tions by  the  way  ? (4)  How  may  age  or  other  circumstances 
peculiar  to  the  patient  influence  the  course  of  his  disease? 
(5)  How  will  this  or  that  treatment  alter  the  outlook? 


280  PROGNOSIS 

In  lobar  pneumonia  age,  physical  type,  personal  habits, 
previous  health,  extent  of  lung  involvement,  the  pulse- 
temperature-respiration  ratio,  the  presence  or  absence  of 
cyanosis,  the  leucocyte  count,  the  type  of  pneumococcus 
all  have  a bearing  on  prognosis.  Specific  chemotherapy  and 
penicillin  have  introduced  another  favourable  factor.  As  a 
useful  background  we  know  that  in  the  majority  of  cases 
the  disease  will  have  terminated  within  ten  days  and  that  in 
this  country  the  general  recovery  rate  before  the  arrival  of 
the  new  remedies  was  about  80  per  cent.,  with  a favourable 
variation  in  childhood  and  adolescence  and  an  adverse 
variation  towards  and  after  middle  life. 

Hour-to-hour  observation  in  one  disease,  day-to-day  or 
week-to-week  observation  in  another,  may  modify  opinion. 
The  information  necessary  for  accurate  assessments  is  often 
available  if  carefully  sought  for.  In  ninety-nine  cases  a boil 
on  the  neck  gives  us  no  great  anxiety,  but  we  must  never  for- 
get that  through  natural  accident  or  ill-judged  treatment  the 
hundredth  may  give  rise  to  a metastatic  renal  abscess  or  a 
fatal  septicaemia.  A cancer  of  the  stomach  may  be  operable 
or  inoperable.  Depending  upon  its  position  and  rate  of 
growth  it  may  run  a variety  of  courses,  with  or  without  pain, 
with  or  without  obstruction,  with  or  without  severe  anaemia. 
We  need  to  know  and  should  try  to  forecast  the  likely 
course  in  each  case,  however  hopeless  the  ultimate  issue 
may  be. 

Books  and  teachers  can  tell  us  a great  deal,  but  our  own 
senses  and  the  experience  of  the  years  tell  us  a great  deal 
more.  Prognostic  ability  of  high  grade  can  only  come  with 
long  experience,  but,  clearly  too,  the  earlier  wc  begin  to 
practise  prognosis  in  a systematic  manner  the  better  it  will 
be  for  our  minds,  for  our  patients,  and  for  the  trust  which 
they  impose  in  us.  This  practice  is  a part  of  what  I frequently 
refer  to  as  * clinical  discipline*,  and  the  best  discipline,  when 
teaching  has  provided  the  rudiments,  is  self-discipline.  We 
must  set  ourselves  standards  in  observing,  in  note-taking, 
and  in  critical  commentary.  We  must  always  prefer  facts 
to  opinions.  If  we  say  or  hear  a teacher  say,  ‘I  believe  this 
patient  will  get  well*,  we  must  proceed  to  discover  and 


287 


PROGNOSIS 

analyse  the  reasons  upon  which  that  opinion  was  based,  and, 
if  it  proves  correct,  to  review  the  significance  of  the  signs 
which  instructed  the  belief.  In  subsequent  cases  of  the  same 
kind  we  are  then  able  to  test  our  experience  and  by  degrees 
to  appreciate  which  clinical  phenomena  have  acquired  a 
positive  or  negative  value. 

The  Influence  of  Prognosis  on  the 
Assessment  of  Treatments 
I have  hinted  ahead}'  that  we  have  no  right  to  conclude 
that  a particular  treatment  is  effective  in  a particular 
disease  unless  we  have  first  familiarized  ourselves  with  its 
natural  prognosis  or  its  prognosis  under  conditions  of  purely 
symptomatic  treatment.  Neglect  of  this  simple  principle  has 
been  responsible  for  countless  misjudgements  and  a great 
waste  of  time  and  money,  and  has  caused  inconvenience, 
discomfort,  and  even  death  to  a large  number  of  patients. 
I have  dealt  with  this  subject  elsewhere,1  but  must  make  a 
further  brief  reference  to  it  here.  Gull  showed  as  long  ago 
how  to  avoid  large  errors  in  therapeutic  judgement  when, 
in  answer  to  some  of  his  contemporaries  who  claimed  that 
they  had  specific  remedies  for  rheumatic  fever,  he  devised 
the  simple  experiment  of  treating  a series  of  cases  with  mint- 
water.  He  was  thus  able  to  show  that  'the  mortality  and 
morbidity  were  no  worse  and  the  duration  of  fever  no  longer 
in  his  cases  than  in  theirs  and  that  their  claims  were  thus 
unsubstantiated.  In  brief,  he  studied  the  natural  prognosis 
of  the  disease  and  thereby  corrected  fallacies.  Vaccines, 
sera,  operations,  and  proprietary  remedies  galore  have  been 
employed  and  arc  still  employed  in  the  same  indiscriminate 
way  as  Gull’s  contemporaries  employed  their  cures  for 
rheumatic  fever  and  with  as  complete  a disregard  for  the 
lessons  of  natural  prognosis.  Only  when  a treatment  has  a 
physiological  basis  proved  by  animal  and  human  experiment 
(as  in  the  case  of  insulin  and  liver-therapy)  or  when,  with 
its  physiological  or  pharmacological  basis  still  to  be  proved 
(as  in  the  case  of  sulplionamides,  penicillin,  and  quinine) 
1 ‘Prognosis  and  Therapeutic  Principle*’  (Brit.  Mtd.  Joum.,  1035,  ii. 
1067). 


288  PROGNOSIS 

large-scale  comparisons  are  possible  between  the  natural 
and  the  modified  prognosis,  are  real  advances  in  therapeutics 
made.  A few  years  ago  an  injection  reputed  to  assist  the 
cure  of  peptic  ulcers  was  launched  with  rosy  claims  but  with 
quite  inadequate  experimental  proofs  and  with  no  prelimi- 
nary clinical  trials.  For  a year  or  more  it  had  a great  vogue. 
Now  it  is  never  heard  of.  Those  physicians  who  at  first 
advocated  it,  claiming  that  at  least  it  relieved  symptoms 
quickly,  overlooked  entirely  the  elementary  fact  that  ulcer 
symptoms  undergo  spontaneous  remission  with  great  fre- 
quency and  in  duodenal  ulcers  almost  with  regularity.  They 
did  not  know  the  natural  prognosis  of  the  disease.  Surgeons 
and  endocrinologists  have  discussed  the  merits  of  operation 
and  hormone  therapy  in  the  treatment  of  undescended 
testicle.  Some  years  ago  I had  the  pleasure  of  reading  a 
thesis  written  by  a school  medical  officer.  Dr.  L.  S.  Marshall, 
of  Taunton,  who  showed  that  in  a series  of  1,910  schoolboys, 
ranging  in  age  from  5 to  1C  years,  undescended  testicle  was 
observed  in  5*1  per  cent.  Of  these  just  over  a half  showed 
bilateral  non-desccnt.  Spontaneous  descent  occurred  before 
puberty  in  95-7  per  cent,  of  cases.  Without  basic  knowledge 
of  this  kind  no  sound  conclusions  could  be  drawn  in  regard 
either  to  the  new  or  the  older  method  of  treatment.  Thera- 
peutic enthusiasm  and  bias  are  dangerous.  The  study  of 
natural  prognosis  is  a corrective  to  both. 

The  Influence  of  Diagnosis  on  Prognosis 
It  might  seem  absurd  to  discuss  the  effect  of  diagnosis  on 
prognosis.  Clearly  an  accurate  prognosis  cannot  be  made  if 
the  diagnosis  on  which  it  is  based  is  wrong.  A diagnosis  may, 
however,  be  correct  in  name  but  only  partially  correct.  A 
patient  may  consult  you  with  angina  pectoris.  If  the  symp- 
toms be  due  to  an  underlying  anaemia  or  anxiety  or  have  a 
slight  physical  basis  with  a large  nervous  aggravation  and 
you  give  him  the  prognosis  due  to  a case  with  advancing 
coronary  disease,  you  will  not  only  give  a wrong  prognosis 
but  you  will  also  do  your  patient  harm  (1)  through  denying 
him  the  correct  treatment  and  (2)  through  increasing  an 
existing  anxiety.  Angina  pectoris,  in  fact,  is  not  a diagnosis 


PROGNOSIS 


289 

but  a symptom.  A familiar  nomenclature  used  as  a diagnosis 
commonly  influences  prognosis  and  treatment  adversely. 
Here  are  cases  in  illustration  of  these  points: 

Case  2.  A man  in  the  middle  fifties  had  been  troubled  for  two  and 
a half  years  with  effort  angina.  Prior  to  its  development  he  had 
passed  through  a period  of  very  considerable  anxiety  and  had  lost 
a near  relative  from  heart  failure.  He  had  restricted  his  activities 
to  an  extreme  degree,  having  previously  led  a very  active  life.  He 
and  his  wife  were  both  unhappy  and  anxious.  No  contra-indications 
to  a good  prognosis  and  increased  activity  were  found  on  the  physical 
side.  Psychologically  a good  prognosis  seemed  to  be  the  wisest 
prescription.  From  that  moment  improvement  was  steady,  and  four 
years  later  he  was  reported  to  be  in  good  health  and  busily  employed 
in  many  useful  ways. 

Case  8.  I was  consulted  by  two  very  anxious  parents  on  behalf  of 
their  small  boy,  aged  7,  who  had  frequently  recurring  seizures  with 
transient  loss  of  consciousness.  I had  no  doubt  tliat  they  were  allied 
to  epilepsy,  but  they  were  different  both  in  their  description  and  in  their 
great  frequency  (up  to  18  fits  a day)  from  ordinary  epileptic  attacks. 
On  this  account  I took  a reassuring  line  and  redoubled  the  reassurance 
when  I learned  from  Sir  Charles  Symonds  that  the  description  I was 
able  to  give  him  was  that  of  pyknolepsy,  a variety  of  seizure  which 
I had  not  previously  encountered  and  from  which  recovery  is  usually 
complete  by  puberty.  Ten  years  later  I received  a grateful  letter 
from  the  mother  to  say  that  the  prognosis  had  been  fully  justified 
and  that  the  boy  had  been  completely  strong  and  well  and  liad 
entirely  outgrown  the  attacks  from  the  age  of  13. 

Once  more  an  epileptiform  attack  is  only  a symptom  or 
syndrome  and,  like  angina  pectoris,  may  carry  very  different 
prognoses.  These  in  their  turn  must  influence  the  lives  and 
happiness  of  patients  for  better  or  for  worse. 

The  Influence  of  Treatment  on  Prognosis 

The  influence  of  specific  treatments  on  prognosis  can  be 
assessed  with  considerable  accuracy,  provided  we  recognize 
the  effects  of  such  variables  as  age,  the  duration  of  the  illness, 
and  the  expert  knowledge  of  those  in  charge  of  the  treatment. 

It  is  almost  impossible  to  measure  the  influence  of  symp* 
tomatic  treatment  on  prognosis.  Can  a timely  hypnotic  or 
stimulant  save  life  ? Can  a gentle  and  a skilful  nurse  or  u 
cheerful  sensible  doctor  make  a difference  between  life  and 
death,  as  compared  with  a dour  and  clumsy  nurse,  or  a dull 

u 


290  PROGNOSIS 

and  careless  doctor  ? Such  questions  we  cannot  answer  with 
proofs,  but  we  find  it  hard  to  doubt  that  the  summary  of 
symptomatic  ministrations  frequently  determines  or  hastens 
recovery.  Well-timed  and  well-chosen  surgical  treatment 
or  specific  therapy  can  undoubtedly  and  in  numerous 
circumstances  save  lives  that  would  otherwise  be  lost,  but 
withholding  surgery  and  specific  treatment  in  certain 
circumstances  may  also  improve  prospects. 

The  real  personal  difficulties  arise  in  those  cases  in  which 
the  arguments  for  or  against  operation  or  a drastic  measure 
of  treatment  are  evenly  balanced.  Then  the  simplest  and 
most  direct  question  we  can  put  to  ourselves  is  this:  ‘Are 
the  risks  of  this  operation  or  treatment,  on  the  evidence 
before  me,  less  or  greater  than  those  of  the  disease  left  to 
Nature  and  symptomatic  methods  ? * Operation  is  the  treat- 
ment of  choice  in  appendicitis,  but  there  are  cases  and  stages 
and  complications  of  appendicitis  in  which  prognosis  (even 
though  the  symptoms  are  very  anxious)  is  better  with  delay 
than  with  immediate  action.  A treatment,  in  fact,  should 
not  be  employed  because  it  is  the  official  treatment  for  the 
disease  from  which  your  patient  is  suffering,  but  because 
you  believe  his  particular  prognosis  wifi  be  improved  by  it. 

Again,  in  anxious  situations  it  is  reasonable  to  pause  and 
ask  oneself:  ‘Would  I wish  this  method  to  be  employed  if 
my  own  wife,  mother,  or  child  were  the  patient  ? ’ In  asking 
this  question  we  help  to  balance  belief  in  a method  or  its 
advocates  against  personal  responsibility  subjected  to  its 
sternest  test,  thereby  weighing  prognosis  in  the  most  critical 
scale  that  conscience  can  devise. 

Temperament,  Anxiety,  and  Prognosis 

There  can  be  no  doubt  that  the  emotional  qualities  of 
the  physician  may  considerably  colour  his  judgements.  I 
had  a good  friend,  now  dead,  who  was  an  able  diagnostician 
but  noted  for  his  gloomy  prognostications.  Although  his 
reputation  was  large  he  must  have  lost  not  a little  practice 
in  proportion  to  the  loss  of  hope  which  he  unwittingly 
engendered  in  the  hearts  of  patients  and  their  doctors.  Men 
like  Sir  William  Gull,  Sir  James  Goodhart,  and  Sir  William 


291 


PROGNOSIS 

Osier — all  great  and  wise  physicians — were  reasoning 
optimists  and  their  practices  were  large  in  proportion  to 
their  generous  natures  and  forecasts. 

There  is  not  one  among  us,  however,  who  can  escape  the 
influence  of  anxiety  in  harassing  situations,  and  anxiety 
cripples  judgement.  This  is  at  no  time  better  manifest  than 
when  sickness  comes  to  the  doctor’s  family.  With  rare 
exceptions,  doctors  find  themselves  incapable  of  sound 
judgements  about  their  own  wives  and  children,  and  prefer 
to  summon  the  help  of  colleagues.  An  illness  which  would 
cause  no  alarm  in  a neighbour's  wife  can  bring  to  mind  all 
the  gravest  complications  in  your  own. 

There  are,  however,  many  other  occasions  in  the  course 
of  practice  in  which  anxiety  is  so  great  as  to  hamper  decision. 
Here  again  self-discipline  may  lend  a helping  hand,  and  by 
sitting  down  to  the  facts  of  the  case  in  the  evening  (remote 
from  the  appeals  of  an  unhappy  household  and  the  threaten- 
ing outward  aspect  of  the  illness  itself),  by  totting  up  the 
favourable  and  unfavourable  features,  recalling  past  experi- 
ence or  talking  the  problem  over  with  a friend  or  partner, 
reason  is  recalled  and  we  nre  enabled  to  give  a just  prognosis, 
carrying  its  message  of  hope  in  one  case  or  regretful  antici- 
pation of  further  anxious  days  or  weeks  in  another.  Both 
in  diagnostic  and  prognostic  problems  I have  occasionally 
resorted  to  a sheet  of  paper  and  set  down  the  ‘plus’  and 
* minus  ’ marks  in  two  columns,  not  expecting  a mathematical 
decision  therefrom,  but  just  as  a means  of  balancing  my 
thoughts. 


Prognostic  Method 

It  would  require  a book  rather  than  a chapter  to  describe 
the  rules  of  guidance  appropriate  to  the  prognosis  of  the 
various  types  of  disease.  Let  me  take  just  one  example 
before  I conclude,  one  which  will  frequently  be  encountered 
in  practice,  which  has  many  anxious  complications,  but 
which  is,  on  the  whole,  too  gravely  regarded  by  doctors  and 
much  too  gravely  by  the  laity.  It  is  one  which  should  have 
a special  interest  for  Guy’s  men  in  that  its  morbid  anatomy 
was  fust  thoroughly  investigated  by  Richard  Bright,  while 


292  PROGNOSIS 

its  clinical  and  pathological  aspects  were  successively 
studied  by  Gull,  Wilks,  and  Mahomed  after  him.  Originally 
included  under  the  heading  of  Chronic  Bright’s  Disease,  it  is 
now  more  usually  referred  to  as  Hypertension,  or  preferably 
Hyperpiesia,  or  simply  as  High  Blood  Pressure.  Here  is  a 
disease  with  a slow,  insidious  course,  with  a liability  to 
death  in  the  long  run  from  cerebral  haemorrhage,  congestive 
heart  failure,  coronary  occlusion,  or  combined  cardio-renal 
failure. 

The  age,  weight,  sex,  occupation,  mentality,  mode  of 
life,  and  family  history,  the  symptoms  and  physical  findings 
in  the  individual  case  may  all  influence  prognosis.  The 
judgements  are  built  upon  clinical  experience  and  morbid 
anatomy.  Is  it  possible  to  balance  the  evidence  in  such  a 
way  as  to  impart  a useful  degree  of  accuracy  to  our  opinions  ? 

If  the  patient  is  a man  aged  50  and  Ids  forebears  have 
died  suddenly  of  strokes  or  heart  failure  during  or  before  the 
sixth  decade,  if  he  is  overweight  and  lives  too  well  or  works 
too  hard  his  prognosis  is  likely  to  be  worse  than  that  of  a 
man  of  the  same  age  with  the  same  blood  pressure,  but  who 
is  lean  and  lives  carefully  and  has  a negative  family  history, 
or  of  a woman  of  the  same  age  who  has  developed  the  high 
pressure  of  the  menopausal  years. 

But  let  us  confine  ourselves  in  this  instance  to  objective 
findings  and  see  if  we  can  usefully  place  our  patient  in  one 
or  other  of  four  prognostic  categories  which  have  seemed  to 
me  convenient  and  useful  in  these  difficult  assessments. 

In  the  first  category  the  patient  has  been  discovered  to 
have  a high  blood-pressure  in  the  course  of  a life  assurance 
examination  or  has  presented  himself  with  minor  symptoms 
of  fatigue  or  irritability.  His  systolic  pressure  on  more  than 
one  occasion  is  170,  his  diastolic  100  mm.  of  mercury.  His 
radial  arteries  are  not  appreciably  hard,  his  apex  beat  is 
within  Che  nipple  line,  his  retinal  arteries  are  barely  beginning 
to  dint  the  veins.  His  urine  is  of  low  specific  gravity,  but 
contains  no  albumen.  He  has  had  no  warning  signals  and 
has  developed  no  appreciable  structural  changes  in  heart, 
arteries,  brain  or  kidneys.  His  diastolic  reading,  which  helps 
to  tell  the  state  of  the  arterial  wall,  has  not  risen  unduly. 


PROGNOSIS  203 

There  is  no  need  to  give  a gloomy  prognosis.  He  may  live 
ten  years  without  illness  or  vascular  accident.  Weight 
reduction,  if  needed,  sensible  modifications  of  life  and  good 
holidays  should  nevertheless  be  counselled. 

In  the  second  category  the  artery  is  palpably  thickened, 
the  systolic  pressure  is  220  and  the  diastolic  pressure  110  to 
120,  the  apex  beat  is  half  an  inch  outside  the  nipple  line, 
there  is  a solitary  retinal  haemorrhage  and  the  urine  contains 
a trace  of  albumen.  Minor  secondary  changes  have,  in  other 
words,  began  to  appear.  There  are  still  no  major  warnings 
of  catastrophe,  but  it  has  become  likely  that  a more  serious 
damage  to  brain  or  heart  will  follow  in  the  next  two  to  five 
years.  Careful  modifications  of  habit  may  still  diminish 
risks  and  postpone  the  evil  day,  but  the  prognosis  must  now 
be  more  guarded. 

In  the  third  category  a vascular  accident  affecting  an 
important  organ,  a coronary  or  cerebral  thrombosis  or  a 
cerebral  haemorrhage,  has  occurred,  or  the  earliest  symp- 
toms of  congestive  failure  have  announced  themselves. 
Perhaps  Cheyne-Stokes  breathing  is  noticed  on  the  consult- 
ing-room couch  or  there  have  been  attacks  of  nocturnal 
dyspnoea  in  threat  of  left  ventricular  defeat.  The  diastolic 
pressure  has  risen  to  140  or  150.  There  are  several  haemor- 
rhages and  white  patches  in  thefundi.  There  is  a heavy  cloud 
of  albumen.  Periods  of  rest  in  bed  have  become  necessary. 
Improvements  are  temporary  and  incomplete.  Death  within 
a year  has  become  probable. 

In  the  fourth  category  our  patient  is  bedridden  with  heart 
failure  and  oedema  or  the  progressive  mental  deterioration 
of  cerebral  arteriosclerosis.  There  has  been  a fall  in  the 
systolic  pressure,  but  the  diastolic  figure  remains  too  high. 
Days  or  weeks  or,  at  the  most,  months  is  the  best  foreeast 
we  can  offer. 

At  each  of  these  stages  advice  and  treatment  must  be 
determined  by  the  prognosis  which  we  construct  from  a 
combination  of  clinical  experience  with  pathological  insight. 
At  no  stage  is  the  construction  of  the  prognosis  merely  an 
academic  exercise.  But  how  often  is  the  pathological  insight 
lacking  and  how  many  patients  are  worried  into  a quite 


204  PROGNOSIS 

unnecessary  anxiety  and  ill-health  because  of  this  lack. 
The  world  is  full  of  unhappy,  careful,  middle-aged  people 
who  would  have  remained  active  for  many  more  years  had 
not  doctors  ascribed  to  a column  of  mercury  a degree  of 
prognostic  reliability  which  it  can  never  alone  possess,  and 
forgotten  both  their  morbid  anatomy  and  the  importance 
of  studying  ‘the  whole  man’. 

Conclusion 

I had  almost  omitted  to  mention  prognosis  as  an  academic 
exercise,  so  many  practical  lessons  have  I found  for  it.  Let 
us  add  now  that  anything  in  our  work  which  trains  the  senses 
and  sharpens  the  wits,  compels  discussion,  invites  analysis, 
and  excites  interest,  also  brings  gifts  to  intellect  and  persona- 
lity over  and  above  the  general  gifts  of  a professional  life. 
It  helps  to  satisfy  a hunger  and  to  nourish  clear  thought  and 
to  foster  that  spirit  of  natural  philosophy  which  should  find 
a home  in  the  heart  of  every  physician.  I would  therefore 
commend  the  study  of  prognosis  as  a salutary  exercise,  as 
an  individual  adventure  in  consecutive  pathology,  and 
suggest  for  serious  consideration  that  the  follow-up  investi- 
gation, be  it  private  or  institutional,  and  the  wider  use  of 
statistical  analyses  have  many  far-reaching  contributions  to 
make  to  medical  knowledge.  In  the  years  ahead  they  must 
be  regarded  as  essential  activities  of  all  hospitals  and  clinics. 

For  the  individual  student  it  would  be  no  bad  exercise  to 
include  a footnote  on  estimated  prognosis  at  the  beginning 
of  every  case-report,  with  a correction  when  possible  at 
the  end. 


XXI 

THE  RADIAL  PULSE1 


From  the  earliest  times  the  examination  of  the  pulse  at  the 
wist  has  been  a familiar  and  important  medical  ritual.  It 
has  lost  nothing  of  its  importance  and  remains  the  most 
frequent  of  the  scientific  observations  of  daily  practice.  I 
say  ‘scientific’  for,  in  counting  the  pulse,  we  are  making  an 
accurate  numerical  record  which  may  be  compared  with 
known  standards,  and  the  personal  equation  plays  no  such 
part  ns  it  does  in  the  assessment  of  many  signs  and  symp- 
toms. In  determining  the  qualities  of  the  pulse  we  may 
make  other  valuable  observations,  but  our  estimates,  not 
being  measurable  by  the  unaided  finger,  lack  precision. 

In  a slender  volume  by  William  Heberden,  with  the  com- 
prehensive title — Commentaries  on  the  History  and  Cure  of 
Diseases — is  included  a small  paper  which  I often  peruse 
with  pleasure.  Its  subject  is  ‘Remarks  on  the  Pulse’,  nnd 
it  was  read  at  the  College  of  Physicians  on  7 July  1768.  It 
has  not  attracted  the  attention  rightly  given  to  his  account 
of  angina  pectoris,  the  first  and  best  account  ever  written 
of  that  disorder,  but  like  so  many  of  Heberden’s  writings 
it  is  remarkable  for  the  accuracy  of  its  clinical  descriptions, 
for  the  soundness  of  its  conclusions,  and  for  the  pleasing 
simplicity  of  its  style.  It  interests  me  to  think  how  gratified 
Heberden  would  be,  if  he  were  to  return  to-day,  to  find  so 
many  of  his  opinions  unaltered  by  the  passage  of  time.  How 
eagerly,  too,  he  would  accept  and  welcome  the  newer  and 
more  certain  knowledge  which  has  been  won  through  the 
agency  of  instrumental  device. 

It  is  well  for  us  to  take  stock  occasionally  of  what  has 
been  added  to  our  store  by  the  introduction  of  methods  and 
instruments  of  precision.  Physicians,  even  if  they  handle 
none  of  these  but  the  sphygmomanometer,  must  remain  in 
constant  debt  to  Sir  James  Mackenzie,  Sir  Thomas  Lewis, 
and  others,  for  the  light  which  their  researches  have  throw 
upon  many  familiar  and  other  less  familiar  pulse  pheno- 

1 Gvy’t  Itoxp.  Gaulle,  1030,  xUv.  SO. 


200  THE  RADIAL  PULSE 

mena.  It  would,  I believe,  be  perfectly  fair  to  claim  that 
we  can  now,  as  a rule,  get  on  very  well  in  practice  without 
the  sphygmograph,  the  polygraph,  or  the  electrocardio- 
graph, but  our  ability  to  do  so  is  in  great  part  due  to  what 
we  have  learned  from  them,  and  in  certain  situations  we 
shall  continue  to  require  their  aid  if  we  are  to  give  of  our 
best  in  diagnosis,  prognosis,  and  treatment. 

My  present  plan,  however,  is  not  to  inquire  into  this 
indebtedness  or  to  discuss  the  physiology  of  the  radial  pulse, 
but  rather  to  consider  what  diagnostic  information  can  be 
obtained  by  us,  employing  only,  after  the  manner  of  Hcbcr- 
den,  the  unaided  finger  and  the  radial  arteries  of  our  patients. 
By  ‘diagnostic  information’  I mean  such  as  will,  without 
further  ado,  allow  a positive  diagnosis  or  strongly  support 
or  suggest  a diagnosis.  I need  hardly  add  that  we  should 
never  rest  content  with  this  evidence  alone,  and  that  my 
purpose  is  rather  to  indicate  how  helpful  so  simple  a pro- 
cedure as  feeling  the  pulse  may  sometimes  be  than  to 
encourage  undue  reliance  upon  it. 

There  are  five  particular  observations  which  may  be  made 
on  the  pulse,  some  of  which  we  make  consciously  or  half- 
consciously  every  time  we  put  a finger  to  a wrist,  but  all  of 
which  in  certain  types  of  case  we  should  be  at  pains  to  make 
and  to  record.  I refer  to  (I)  the  rate,  (2)  the  rhythm,  (8)  the 
volume,  (4)  the  tension  of  the  pulse,  and  (5)  the  state  of  the 
artery . 

For  convenience,  however,  I shall  here  consider  abnor- 
malities of  pulse  behaviour  under  three  headings,  namely, 
altered  rate,  altered  rhythm,  and  altered  quality — allowing 
quality  to  speak  for  volume,  tension,  and  the  state  of  the 
vessel.  You  will  appreciate  that  rate,  rhythm,  and  quality 
may  be  severally  or  simultaneously  modified.  You  will  also 
observe  that  pulses  may  be  diagnostic  of  general  as  well  as 
of  cardiovascular  diseases. 

Altered  Rate 

Heberden,  wisely  partial  to  matters  of  fact,  devotes  a 
large  part  of  his  paper  to  pulse-rate  or  frequency.  We  all 
know  that  the  rate  of  the  pulse  in  health  varies  with  age, 


208  THE  RADIAL  PULSE 

year  or  two  ago  with  basal  congestion  and  slight  haemo- 
ptysis in  which  my  house  physician  feared  pneumonic 
tubercle,  but  the  history  and  the  pulse  peculiarity,  with  a 
rate  of  150,  in  a patient  seeming  singularly  little  perturbed, 
suggested  some  form  of  paroxysmal  tachycardia,  and  this 
was  proved  by  an  electrocardiogram  to  be  due  to  ‘flutter’. 
Very  high  rates  and  sometimes  paroxysmal  behaviour  also 
occur  with  auricular  fibrillation.  With  the  high  rates  it  is 
often  difficult  to  appreciate  the  presence  of  arrhythmia.  A 
woman,  aged  54,  had  a pulse-rate  in  my  consulting-room  of 
ICO  to  the  minute  and  over,  and  (as  I noted  it  at  the  time) 
the  pulse  was,  so  far  as  the  finger  could  determine,  ‘practi- 
cally regular’.  But  her  bouts,  as  she  described  them,  did 
not  end  abruptly,  the  tachycardia  had  now  become  persis- 
tent, and  her  appearance  suggested  organic  heart-disease. 
An  electrocardiogram  showed  auricular  fibrillation,  and 
she  responded  very  well  to  digitalis.  When,  therefore,  the 
clinical  features  do  not  accord  with  a simple  paroxysmal 
tachycardia  we  must  have  the  assistance  of  an  electrocar- 
diogram, for  without  it  appropriate  and  valuable  treatment 
cannot  be  happily  instituted  and  controlled. 

Bradycardia , with  pulse-rates  in  the  neighbourhood  of 
or  just  below  50,  occurs  in  some  big,  robust  men  in  health; 
after  certain  fevers ; with  jaundice,  starvation,  and  cerebral 
compression ; and  sometimes  in  myxoedema ; but  in  none  of 
these  is  the  pulse-rate  alone  diagnostic.  A pulse-rate  of  80 
or  less,  however,  nearly  always  means  complete  heart-block, 
and  so  enables  us  to  diagnose,  with  a finger  on  the  wrist,  a 
lesion  of  the  auriculo-ventricular  bundle.  It  may  so  serve 
to  explain,  without  further  inquiry,  fainting  attacks  or  fits 
which  had  otherwise  remained  obscure.  To  feel  the  uncom- 
fortable pause  between  beats  in  these  cases  is  a strange 
experience  and  not  easily  forgotten. 

Altered  Rhythm 

Other  alterations  of  rhythm  may  be  correctly  assessed 
with  a finger  on  the  wrist,  but  I shall  only  dwell  upon  one 
significant  and  one  less  significant  type  of  arrhythmia,  both 
of  them  common  in  practice. 


000  THE  RADIAL  PULSE 

that  they  are  not  worth  regarding  in  any  illness,  unless  joined  with 
other  signs  of  more  moment.  They  are  not  uncommon  in  health,  and 
are  often  perceived  by  a peculiar  feel  at  the  heart  by  the  persons 
themselves  every  time  the  pulse  intermits.* 

Actually  I suspect  that  it  is  the  compensatory  pause  which 
gives  the  ‘peculiar  feel  at  the  heart*.  He  even  pursued  to 
necropsy  the  case  of  a woman  dying  of  cancer  who  had  had 
an  intermitting  pulse  from  her  youth,  and  ‘nn  able  anato- 
mist’ could  demonstrate  no  disease  of  the  heart,  pericar- 
dium, or  great  vessels. 

In  diagnosing  extra-systoles,  therefore,  you  are  often  in 
the  happy  position  of  being  able  to  diagnose  something  that 
does  not  much  matter  and  so  can  the  better  reassure  your 
patient. 

Altered  Quality 

There  is  a remarkable  type  of  pulse  associated  with  the 
name  of  Corrigan,  a Dublin  physician,  and  alternatively 
described  as  the  water-hammer  pulse,  which  is  characteristic 
of  incompetence  of  the  aortic  valve.  It  is  best  felt,  not  with 
the  finger-tips,  but  with  the  palmar  aspects  of  the  fingers 
laid  across  and  embracing  the  flexor  aspect  of  the  patient’s 
wrist  and  with  his  arm  raised  above  the  level  of  his  chest. 
It  can  frequently  be  recognized  without  this  manoeuvre, 
but  with  it  the  peculiar  shock-like  sensation  accompanying 
the  sharp  thrust  and  quick  recoil  of  the  artery  are  better 
appreciated,  and  the  ulnar  pulse — not  as  a rule  easily  found 
— is  simultaneously  felt.  I find  that  most  of  my  clerks  have 
no  idea  as  to  why  it  is  called  a ‘water-hammer’  pulse.  A 
water-hammer  is  a physical  toy  and  consists  of  a glass  tube 
half  filled  with  water  from  which  the  air  has  been  largely 
exhausted.  When  it  is  tilted  the  water  falls  with  a peculiar 
slap  to  the  other  end  of  the  tube,  so  that  the  name  is  quite 
appropriate.  Pulses  of  water-hammer  type  are  also  felt  in 
severe  anaemias,  especially  in  the  recovery  phase  after 
recent  haemorrhage,  and  frequently  also  in  elderly  folk  with 
rigid  thoracic  aortas.  But  in  its  most  developed  form  the 
water-hammer  pulse  proclaims  an  aortic  leak.  Aortic  in- 
competence is  a result  of  rheumatic  or  infective  endocarditis 
or  syphilitic  aortitis. 


THE  RADIAL  PULSE  SOI 

Aortic  stenosis  also  has  a peculiar  and  characteristic  pulse, 
although  it  is  not,  as  a rule,  so  readily  appreciated  as 
Corrigan’s  pulse.  Unlike  the  latter  ■which  we  may  visualize, 
in  a sphygmographic  way,  as  a sudden  ascent,  a sharp  peak, 
and  a swift  decline,  the  stenotic  pulse  conveys  the  impres- 
sion of  a plateau-like  curve.  In  other  words,  it  takes  time 
to  pass  the  palpating  finger.  For  this  reason  it  is  still  better 
felt  with  two  approximate  fingers  simultaneously.  I know 
of  no  other  condition  which  will  produce  this  kind  of  pulse. 

The  pulse  of  high  blood-pressure. — There  is  no  more  charac- 
teristic pulse  in  medicine  than  the  high-tension  pulse,  the 
pulsus  magnus,  durus,  et  tardus,  of  the  older  physicians. 
Unless  cardiac  defeat  has  supervened  upon  long  hyperpiesia 
the  pulse  is  slow  and  generally  of  full  volume,  but  what 
is  especially  remarkable  is  the  degree  of  finger-pressure 
necessary  to  obliterate  the  pulse-wave  so  that  it  cannot  be 
felt  by  another  finger  at  a lower  level.  The  artery  itself  in 
later  stages  of  the  disease  imparts  a sensation  of  toughness 
or  hardness  to  the  finger,  can  be  felt  and  rolled  even  when 
the  pulse  is  obliterated,  and  is  commonly  tortuous.  Ac- 
curate estimation  of  the  blood-pressure  without  the  sphyg- 
momanometer is,  I believe,  impossible  even  with  long 
practice,  but  we  should  generally  be  able  to  estimate  that  a 
systolic  pressure  is  above  180  or  below  100  mm.  of  mercury. 
Between  these  figures  it  is  difficult  to  arrive  confidently 
within  thirty  or  forty  millimetres  of  the  correct  reading. 

In  striking  contrast  is  the  extremely  loro -tension  pulse  of 
Addison’s  disease  which,  when  you  have  had  experience  of 
a case  or  two,  may  be  the  first  thing  to  draw'  attention 
to  the  true  diagnosis.  The  symptoms  in  the  early  stages  of 
the  disease  often  amount  to  little  more  than  a complaint 
of  weakness ; pigmentation  is  not  always  obvious,  and  in  a 
blonde  Saxon  type  I have  known  it  entirely  lacking.  There 
is  something  arresting  and  uncanny  in  the  feel  of  a pulse  so 
weak  and  compressible  in  a patient  perhaps  but  recently 
prevented  from  going  about  his  affairs.  In  later  stages  to 
palpate  is  almost  to  obliterate  the  pulse.  Apart  from  states 
of  syncope  and  collapse  and  certain  cases  of  coronary  occlu- 
sion, an  accident  which  is  usually  associated  with  a pro- 


302 


THE  RADIAL  PULSE 
found  fall  in  blood-pressure,  it  is  quite  uncommon  to  feel 
pulses  of  the  peculiar  poor  quality  which  we  associate  with 
disorganization  of  the  suprarenal  glands,  and  which  Addison 
himself  described  as  ‘small  and  feeble’  or  ‘excessively  soft 
and  compressible’. 

There  is  an  alteration  in  the  pulse  described  as  dicrotism 
in  which  the  dicrotic  wave  is  greatly  exaggerated  and  each 
beat  appears  to  be  duplicated  or  accompanied  by  a poor 
reflection  of  itself.  The  sensation  imparted  to  the  finger  is 
unique,  generally  unmistakable,  and  quite  distinct  from 
that  furnished  by  a bigeminal  pulse  in  which  every  normal 
beat  is  followed  by  a premature  contraction  and  then  by 
a compensator}'  pause.  It  can,  however,  be  mistaken  for 
doubling  of  the  pulse-rate  and  may  be  so  charted  by  the 
nurse.  The  dicrotic  pulse  occurs  especially  in  grave  febrile 
illnesses,  but  is  so  frequent  in  typhoid  fever  and  compara- 
tively so  infrequent  in  other  diseases  that  it  has  long  been 
regarded  as  a ‘diagnostic  pulse*. 

In  a case  to  which  I was  called  last  year,  in  which  severe 
headache  and  high  pyrexia  had  led  to  a fruitless  exploration 
of  the  accessory  sinuses,  a dicrotic  pulse  was  noted  and  was 
the  first  thing  to  suggest  the  actual  diagnosis.  I was  a little 
shaken  and  incredulous  when  the  pathologist,  two  days 
later,  reported  that  he  had  grown  B.  coli  from  the  blood,  but 
wc  had  not  long  to  wait  before  rose-spots  appeared  and 
simultaneously  the  pathologist  revised  his  verdict  and  an- 
nounced B.  paralijphosus  B in  all  cultures.  I have  recently 
had  an  example  of  extreme  dicrotism  in  Addison  Ward  in 
the  case  of  a boy  with  miliary  tuberculosis  with  pericarditis. 
Post  mortem  we  found  miliary  tubercles  throughout  the 
myocardium. 

Complete  pulselessness,  excepting  for  very  short  periods 
or  when  the  artery  is  obliterated,  might  be  thought  to  be 
inconsistent  with  life.  Thus  we  associate  the  condition 
chiefly  with  syncopal  attacks,  with  shock,  haemorrhage,  or 
the  moribund  state.  I have,  however,  the  notes  of  two  cases, 
in  the  first  of  which  no  pulse  could  be  felt  at  the  wrist  for 
some  12  hours,  while  in  the  second  the  radial,  carotid,  and 
subclavian  pulses  were  all  impalpable  for  12  hours  and  the 


THE  RADIAL  PULSE  303 

radial  was  only  doubtfully  palpable  after  24  hours.  Botli 
were  cases  of  anaphylactic  shock  following  administration 
of  serum  and  both  made  a complete  recovery.  (See  Lecture 
XXXIII.) 

John  Hunter  records  that  in  his  first  anginal  seizure, 
which  was  almost  certainly  due  to  a coronary  occlusion, 
four  physicians  were  unable  to  feel  his  pulse  for  the  space 
of  three-quarters  of  an  hour.  He  survived  the  attack  for 
twenty  years.  I know  of  no  other  conditions  in  which  pro- 
longed pulselessness  may  occur  and  yet  recovery  follow. 

A rare  pulse  anomaly  is  the  pulsus  paradoxus,  in  which 
the  pulse  weakens  or  disappears  in  inspiration.  It  is  a sign 
of  pericarditis  with  effusion. 

The  types  of  pulse  which  I have  endeavoured  to  describe 
are  all  definite  in  their  way  and  instructive  for  that  reason. 
Their  value  is  chiefly  diagnostic.  But  there  are  other  less 
definite  pulse-variations,  instructive  rather  in  a prognostic 
way,  which  it  would  be  beyond  my  power  to  describe.  How 
is  it  that  we  visit  a case  sometimes  and,  notwithstanding 
that  the  patient — perhaps  a victim  of  pneumonia  or  some 
surgical  disease — appears  to  be  doing  fairly  well,  we  say 
‘But  I don't  quite  like  the  quality  of  his  pulse',  and  arc 
justified  in  our  anxiety  by  subsequent  events?  And  how  is 
it,  contrarily,  that  we  may  see  a patient  seemingly  in  dire 
straits  and,  largely  on  the  quality  of  his  pulse,  give  a more 
hopeful  verdict?  It  is  not  mere  guess-work  nor  yet  any 
special  skill,  but  rather  the  interpreted  result  of  past  ex- 
perience and  a subconscious  reading  of  rate,  rhythm, 
volume,  and  tension  and  their  relations  to  one  another  and 
to  other  signs.  Such  mental  procedures  cannot  be  taught, 
but  it  is  open  to  us  to  acquire  them  by  self-schooling  in  the 
art  of  observation. 

llcbcrdcn,  criticizing  certain  doctrines  prevalent  in  his 
time,  says: 

*1  have  more  than  once  observed  old  and  eminent  practitioners 
make  such  different  judgements  of  hard,  and  full,  and  weak,  and 
small  pulses,  that  I was  sure  they  did  not  call  the  same  sensations 
by  the  same  names.  It  is  to  be  wished,  therefore,  tliat  physicians, 
in  their  doctrines  of  pulses,  and  descriptions  of  cases,  had  attend  ed 


304  THE  RADIAL  PULSE 

more  to  such  circumstances  of  the  pulse,  in  which  they  could  neither 

mistake  nor  be  misunderstood.’ 

He  was  here  referring  more  particularly  to  the  rate,  but 
if  we  are  clear  also  in  our  use  and  understanding  of  the 
terms  and  systematic  in  our  assessment,  when  occasion 
demands,  of  rhythm,  volume,  tension,  and  the  condition  of 
the  arterial  wall,  we  shall  be  subscribing  still  further  to  this 
wise  behest. 


XXII 


HYPERPIESIA1 

We  owe  to  the  late  Sir  Clifford  Allbutt,  who  devoted  much 
time  and  scholarly  labour  to  the  study  of  arterial  disease  in 
general  and  of  arterial  hypertonus  in  particular,  the  terms 
‘hypcrpiesis’  and  ‘hyperpiesia’.  By  hyperpiesis  we  under- 
stand the  fact  of  raised  blood-pressure;  we  know  that  it 
may  be  transient  or  persistent,  and  that  it  may  accompany 
a variety  of  conditions,  including  arterial  disease,  chronic 
renal  disease,  lesions  causing  increased  intracranial  pres- 
sure, exophthalmic  goitre,  and  so  forth.  By  hyperpiesia 
we  understand  a peculiar  and  interesting  malady  in  which 
raised  blood-pressure  is  the  most  constant  and  outstanding 
feature.  Clifford  Allbutt  described  it  as  a malady  in  which, 
at  or  towards  middle  life,  the  blood -pressure  rises  exces- 
sively— a malady  having  a course  of  its  own,  and  deserving 
the  name  of  a disease.  To  Clifford  Allbutt  we  are  also  in- 
debted for  the  clearing  away  of  much  of  the  confusion 
which  previously  existed  between  hyperpiesia  and  renal 
high  blood-pressure  on  the  one  hand,  and  hyperpiesia  and 
senile  or  ‘decrescent’  atheroma  on  the  other.  In  order  to 
prepare  the  way  for  our  discussion  I have  tabulated  the 
broader  clinical  distinctions  between  these  diseases  in  the 
later  stages  of  their  development. 


Hyperpiesia 

Age-Incidence  . -lO-OO 

Physical  type  . Robust,  healthy 

Urine  . . . Alb.  n(I  or  trace 

Cardiac  hypertrophy  Always  present  latterly 
Elood-urca  . . Not  raised  or  very  slightly  Greatly  raised 

Retinol  changes  . Haemorrhages  and  *wiry’  Albuminuric  retinitis 
vessels 

„ . { Cerebral  haemorrhage  Uraemia 

Death  from  . , de(ral. 

1 Guy's  Ilosp.  Gazette,  1023,  xxjlIx.  5-tO. 

X 


Chronic  Interstitial 
Nephritis 

20-50 

Unhealthy,  anaemic 
Present,  perhaps  copious 
Present,  latterly 


800 

HYPERPIESIA 

Senile  or  ‘Decrescent' 

Hyperpiesia 

Atheroma 

Age-incidence 

. 40-C0 

GO-60 

Artery  . 

. Thick,  tough,  but  not  at 
first  tortuous 

Thick,  hard,  tortuous 

lllood-prossurc 

. Always  raised 

Not  necessarily  raised 

Heart  . 

. Hypertrophied 

Not  necessarily  hyper- 
trophied 

1 Coronary  artcriosclcro- 

Death  from  . 

I Cerebral  haemorrhage 
■ \ ‘Cardiac  defeat’ 

f sis  with  myocardial 

1 degeneration,  or  inter- 
l current  disease 

The  Causes  of  Hypeiipiesia 

Is  the  high  blood-pressure  in  hyperpiesin  due  to  arterial 
disease,  or  is  the  arterial  disease  due  to  the  high  blood- 
pressure?  That  the  high  pressure  is  not  wholly  due  to  the 
arterial  disease  is  apparent  from  the  fact  that  periods  of 
great  improvement  may  occur  in  the  course  of  the  malady, 
and  also  from  the  observation  that  the  blood-pressure  may 
be  temporarily  and  greatly  lowered  by  the  administration 
of  nitrites.  In  other  words,  even  if  arterial  disease  be  present 
from  the  beginning — which  is  doubtful — we  must  also 
imagine  the  presence  of  some  other  factor  which  raises 
blood-pressure  by  stimulating  liypertonus  of  the  arterial 
musculature.  It  is  commonly  supposed  that  some  circulat- 
ing pressor  substance  is  at  work,  and  disputes  occur  as  to 
whether  this  pressor  substance  is  in  the  nature  of  a toxin 
resulting  from  bacterial  action  within  the  bod}',  or  whether 
it  is  a product  of  faulty  metabolism,  or  otherwise  evolved. 
Against  the  bacterial  theory  are  the  observations  that  most 
bacterial  toxins  have  a depressor  effect,  and  that  sufferers 
from  hyperpiesia  are  commonly  robust  and  healthy  looking 
individuals  with  no  discoverable  sign  of  alimentary  or  other 
intoxication. 

Various  careful  researches  have  shown  that  in  cases  of 
hyperpiesia  examined  after  death  there  is  present  in  the 
arteries,  and  more  in  some  arteries  than  in  others,  a definite 
and  constant  histological  change.  To  this  change  Dr.  Geof- 
frey Evans  has  given  the  name  diffuse  hyperplastic  sclero- 
sis. His  work  would  seem  to  suggest  that  diffuse  hyper- 
plastic sclerosis  is  the  pathological  synonym  for  the  clinical 


HYPKFtPIESIA  507 

condition  hyperpiesia.  He  gives  as  the  most  reliable  clini- 
cal evidence  of  hyperpiesia  a systolic  blood-pressure  of  (or 
above)  190  mm.  of  mercury;  and  as  the  most  constant  and 
prominent  morbid  anatomical  finding  cardiac  hypertrophy, 
•with  a heart  usually  weighing  over  15  oz. 

I would  not  have  you  imagine  from  this  that  hyperpiesia 
cannot  be  diagnosed  in  the  presence  of  lower  blood-pressures 
and  in  the  absence  of  clinically  obvious  cardiac  hypertrophy. 
The  disease  should  be  diagnosed,  if  the  patient  presents 
himself  soon  enough,  long  before  such  a stage  has  been 
reached.  We  do  not  really  know  whether  or  not  diffuse 
hyperplastic  sclerosis  is  present  in  the  early  phases  of  the 
disease,  but  we  do  know  that  clinically  the  radial  artery  may 
at  first  show  very  little  thickening  or  hardening. 

Setting  aside  for  the  moment  all  theories  in  regard  to  the 
existence  of  a pressor  substance,  arc  there  any  other  obser- 
vations which  suggest  the  existence  of  other  causal  or  con- 
tributory factors  in  the  development  of  hyperpiesia  ? The 
older  physicians,  having  no  bacteriologists  or  biochemists 
to  instruct  or  bewilder  them,  devoted  much  time  to  the 
study  of  aetiology  and  diathesis.  From  such  studies  they 
often  drew  valuable  conclusions,  and  in  few  chronic  diseases 
does  study  of  this  kind  prove  more  profitable  than  in  the 
case  of  hyperpiesia.  Thus  we  find  evidence  of  a predispo- 
sition to  hyperpiesia  both  in  family  history  and  in  physical 
type,  and  it  lias  long  been  recognized  that  there  is  a very 
definite  age-period  at  which  symptoms  appear,  nnd  within 
which  the  course  of  the  disease  is  laid.  It  is  not  at  all  rare 
to  find  that  cerebral  haemorrhngc  or  henrt  failure  has  been 
a common  cause  of  death  among  the  relatives  or  ancestors 
of  a patient  with  high  blood -pressure,  and  that  these  deaths 
have  for  the  most  part  occurred  between  the  ages  of  fifty 
and  seventy.  The  majority  of  sufferers  from  hyperpiesia  arc 
of  rather  a robust  and  vigorous  type,  sometimes  plethoric, 
sometimes  obese,  although  I think  we  should  also  include 
a lean  and  nervous  type.  For  the  purposes  of  this  lecture  I 
at  one  time  looked  through  the  notes  of  nil  my  patients  with 
high  blood-pressure.  From  these  I excluded  all  cases  in  which 
the  high  blood-pressure  was  due  to  other  apparent  causes, 


mTEnriESiA 


such  as  nephritis  or  Graves’s  disease,  ali  cases  in  which  the 
patient  presented  himself  on  account  of  another  disease, 
and  all  cases  in  which  the  high  pressure  might  have  been  a 
transient  phenomenon,  or  in  which  other  symptoms  or  signs 
of  hyperpiesia  were  lacking.  The  systolic  blood-pressure  was 
170  or  over  in  every'  case  and  the  diastolic  pressure  100  or 
over  in  all  cases  but  one,  cases  with  lower  figures  being  ex- 
cluded for  purposes  of  the  survey.  I obtained  the  following 
figures  in  regard  to  age-incidence  and  physical  type: 

Males,  40%  Females,  54% 

Age — Lowest  . . .21  Lowest  . . . ,28 

Highest  . .08  Highest  . . . .72 

Average  . . .57  Average  . . . .53 


rhydeal  Type  (bath  taxes  together) 


Robust,  healthy,  stout,  plethoric,  or  ‘hypersthenic’  . . 62  per  cent. 

Average 18  „ 

Lean  nnd  nervous  .......  4 „ 

Toor  physique 10  „ 


Other  factors  besides  the  family  history,  age,  and  physical 
type  which  are  commonly  associated  with  hyperpiesia  are 
the  menopause  in  women,  at  which  period  high-pressure 
symptoms  may  manifest  themselves  rather  abruptly*;  hard 
work;  worry;  the  stress  of  modem  life;  and  good  living. 
The  part  played  by  tobacco  and  alcohol  is  doubtful.  The 
information  available  thus  suggests  that  hyperpiesia  should 
at  present  be  regarded  rather  as  a reaction  to  rarious  morbid 
stimuli,  and  occurring  in  individuals  of  the  hypersthenic 
constitution,  than  as  a specific  response  to  a single  specific 
substance.  If  a pressor  substance  is  necessary  for  the 
production  of  the  arterial  hypertonus,  perhaps  we  might 
suggest  that  this  substance  is  activated  through  the  sympa- 
thetic nervous  sy’stem  sometimes  by  over-eating,  over-work, 
or  worry,  sometimes  by  the  endocrine  disturbances  of  the 
menopause  or  by  a combination  of  these  factors,  but  that 
such  activation  is  seldom  effective  unless  there  is  already 
present  a constitutional  or  diathetic  factor. 


Clinical  Features  and  Course 
The  symptoms  which  may  be  complained  of  by  sufferers 
from  hyperpiesia  are  very  numerous,  but  for  the  most  part 


HYPERPIESIA  S09 

they  have  reference  to  the  head  or  the  heart.  In  the  early 
stages  these  symptoms  may  appear  trivial  and  unconvincing 
and  unless  the  blood-pressure  be  taken— and  the  sphygmo- 
manometer must  be  the  arbiter  in  every  suspected  case 
— the  diagnosis  may  well  be  missed  at  a stage  in  which  the 
prospects  of  treatment  ore  most  favourable.  On  the  basis 
of  my  case-notes  I have  tabulated  the  main  symptoms 
exliibited  amongst  a group  of  patients  who  were  for  the 
most  part  sufficiently  well  to  be  up  and  about  and  leading 
moderately  active  or  partially  restricted  lives.  The  few 
exceptions  were  cases  of  cerebral  haemorrhage  or  failing 
heart.  The  frequency  of  the  symptoms  in  the  series  is  given 
as  an  approximate  percentage: 

Main  Subjective  Symptoms 

Per  cent. 


Headaches,  including  pressure  feelings,  ‘bursting  sensations’,  ‘tight 
band  round  head’.  Sec.  ........  45 

Cardiac  symptoms  (Including  dyspnoea,  precordial  pain,  consciousness 

of  heart  throbbing) S3 

Nocturnal  frequency 52 

Dizziness 20 

Nervousness  (Including  anxiety,  fears,  claustrophobia)  . . ,22 

Fatigue 18 

Anginal  pain 10 

Cerebral  vascular  lesions  (symptoms  of) 10 

Ocular  symptoms,  including  sudden  blindness,  failing  vision,  effects  of 
inlrn'ocular  haemorrhages  .......  0 

Epistaxis  6 

Mental  symptoms 0 

Noises  in  head fl 

Haemoptysis 4 


It  will  at  once  be  observed  that  many  of  these  symptoms, 
such  as  hcadaclie,  dizziness,  dyspnoea,  and  nervousness  arc 
common  to  a host  of  other  diseases,  and  that  many  of  them 
may  also  occur  in  patients  without  any  appreciable  evidence 
of  organic  disease  at  all.  The  list  should,  however,  serve  to 
remind  you  how  important  it  is  never  to  neglect  subjective 
symptoms ; and  perhaps  this  is  particularly  the  case  about 
the  middle  period  of  life.  The  mnjorit}’  of  these  sjTnptoms 
sufficiently  explain  themselves.  The  cardiac  symptoms  arc 
a direct  result  of  over-working  of  the  left  ventricle  in  its 
effort  to  combat  the  increased  peripheral  resistance.  The 
nocturnal  frequency  is  probably  due  to  the  high  pressure  in 


310  HYPERPIESIA 

the  renal  arterioles ; the  headaches  and  dizziness  to  increased 
intracranial  pressure ; the  anginal  pain  to  local  sclerosis  of 
the  coronary  arteries;  the  fatigue  symptoms  to  combined 
cardiac  and  cerebral  over-stimulation  and  over-activity ; the 
epistaxis  to  a rupture  of  the  delicate  unprotected  capillaries 
of  the  nasal  mucosa.  The  nervousness,  however,  requires 
more  judicial  consideration,  for  in  some  cases  it  is  very  diffi- 
cult to  say  how  far  a nervous  and  anxious  mind  has  predis- 
posed to  the  hyperpiesia,  or  how  far  the  hyperpiesia  has 
rendered  the  patient  more  liable  to  emotional  unrest.  I have 
small  doubt  that  high  blood-pressure  can  create  in  a pre- 
viously calm  and  phlegmatic  individual  a state  of  mind  in 
which  he  is  easily  perturbed  or  * rattled  ’,  and  in  which  ‘ mole- 
hills* take  on  the  proportions  of  * mountains ’. 

Physical  examination  commonly  shows  the  sufferer  from 
hyperpiesia  to  be  a vigorous  type  of  man  or  woman,  some- 
times looking  so  healthy  that  the  facial  aspect  misleads  into 
an  attitude  of  false  security.  A little  later  in  the  course  of 
the  disease  the  red  cheeks  may  show  an  underlying  tinge 
of  purple,  particularly  in  cold  weather.  In  the  hyperpiesia 
accompanying  the  menopause  there  is  a liability  to  a diffuse 
and  sustained  fluslu'ng  of  the  face  and  neck  during  moments 
of  anxiety  or  fatigue,  which  is,  I think,  an  aggravation  of 
the  ordinary  ‘hot  flushing’  complained  of  at  these  times. 
The  pulse  is  full  and  slow  and  not  readily  compressible — the 
palms  magnus,  durvs,  et  tardus  of  the  old  physicians.  The 
quality  of  resistance  imparted  to  the  fingers  by  the  artery  is 
often  that  of  toughness  rather  than  hardness.  The  apex- 
beat  may  be  found  to  be  in  or  perhaps  just  to  the  left  of  the 
nipple  line.  The  aortic  second  sound  is  accentuated,  some- 
times sharp  or  sometimes  ringing.  The  fundi  may  show 
wiry  and  rather  tortuous  vessels,  perhaps  even  a small 
haemorrhage  or  two.  At  an  early  stage  the  arteries  compress 
the  veins  as  they  cross  them.  The  urine  is  of  low  specific 
gravity,  and  it  may  or  may  not  show  a trace  of  albumin. 

It  is  difficult  to  estimate  the  average  duration  of  the 
disease,  for  we  do  not  in  any  individual  case  know  when  it 
began,  and  the  onset  and  progress  are  insidious  and  the 
course  variable.  Perhaps  some  idea  of  its  natural  stages  may 


IIYFERriESIA  Oil 

be  given  by  providing  you  with  a composite  picture  of  a 
case:  A hard-worked  business  man  discovers  at  fifty  that 
his  pulses  go  a little  too  quickly,  and  that  he  has  slight 
shortness  of  breath  on  exertion,  that  he  has  become  liable 
to  mild  temporal  headaches,  and  that  he  tires  more  easily 
than  he  used  to  do.  Odd  symptoms  of  a minor  kind  may  be 
traced  back  a year  or  two  earlier.  His  blood-pressure  is 
found  to  be  ICO  systolic,  110  diastolic.  His  urine  shows  a 
faint  haze  of  albumin  on  boiling.  He  continues  with  his 
work,  taking  rather  more  care  of  himself  than  before,  and 
a year  or  two  later,  after  a busy  spell,  reports  himself  as 
rather  more  troubled  with  dyspnoea,  and  mentions  occa- 
sional bouts  of  epistaxis.  During  this  time  his  blood- 
pressure  is  found  to  have  risen  to  200  systolic,  180  diastolic. 
He  has  become  rather  irritable ; has  to  get  up  to  pass  water 
twice  at  night;  and  is  annoyed  by  being  unduly  conscious 
of  his  carotid  pulsations  when  lie  lays  his  head  on  the  pillow. 
He  is  persuaded  to  retire  from  his  work  and  to  lead  a quieter 
life.  For  a time  he  shows  definite  improvement,  but  ulti- 
mately, after  a longer  or  shorter  interval,  is  carried  off  by 
a cerebral  haemorrhage,  or  sometimes  less  abruptly  by  what 
Clifford  Allbutt  so  aptly  describes  as  ‘cardiac  defeat’.  The 
period  which  elapses  between  his  first  symptoms  and  his 
death  may  be  anything  between  five  and  fifteen  years  or 
even  longer;  the  symptoms  experienced  during  that  time 
may  be  slight  or  troublesome  or  only  latterly  crippling. 
Often  the  response  of  the  hypertrophied  heart  is  good 
throughout,  and,  without  any  urgent  or  distressing  symp- 
toms ever  having  developed,  death  kindly  closes  the  scene 
with  a sudden  apoplexy.  But  there  is  a rosier  side  to  the 
picture,  for  some  patients  will  support  a systolic  blood* 
pressure  of  180  or  200  for  years,  leading  contented  and  even 
active  lives  and  dying  of  some  other  disease.  Indeed  high 
arterial  pressure  only  becomes  of  serious  moment  when  it 
begins  to  produce  symptoms  of  distress  and  signs  of  struc- 
tural damage  in  other  departments  of  the  body. 

This  lack  of  definite  correlation  between  the  height  of 
the  recorded  pressures  and  the  severity  of  symptoms  brings 
us  necessarily  to  the  discussion  of  what  is  a pathological 


312  HYPERPIESIA 

high  blood-pressure.  Various  methods  are  given  for  assess- 
ing the  average  blood-pressure  at  different  ages.  A simple 
plan  is  to  take  the  systolic  pressure  as  120  at  the  age  of  20 
and  to  add  ten  millimetres  of  mercury  for  each  decade,  but 
some  observers  regard  all  blood -pressures  above  150,  what- 
ever the  age  of  the  patient,  as  pathological.  I should  regard 
a systolic  blood-pressure  of  180  or  upwards  as  pathological 
and  signifying  hyperpiesia  at  any  age,  but  I am  satisfied 
that  it  is  quite  possible,  in  the  presence  of  other  symptoms, 
to  diagnose  hyperpiesia  correctly  with  a blood-pressure  of 
1G0.  I should  be  disinclined  to  diagnose  hyperpiesia  with  a 
blood-pressure  below  150,  excepting  in  a young  subject,  or 
with  a clear  association  of  other  confirmatory  signs  and 
symptoms.  With  the  more  doubtful  borderline  figures  re- 
peated observations  with  the  sphygmomanometer  should 
always  be  made.  The  diastolic  pressure  was  100  or  over  in 
every  case  but  one  in  my  series,  and  110  or  over  in  four-fifths 
of  the  series. 


Differential  Diagnosis 

As  I have  already  shown,  the  differential  diagnosis  must 
be  made  particularly  from  chronic  interstitial  nephritis, 
and  in  the  presence  of  retinal  changes,  much  albumin, 
or  other  suggestive  features,  the  blood-urea  should  be 
estimated,  or  other  renal  efficiency  tests  performed.  High 
blood -pressure  in  young  subjects  should  also  be  more  care- 
fully studied  from  the  renal  point  of  view  than  at  the  more 
usual  age-period  for  the  disease.  The  list  of  symptoms  which 
I have  given  will  remind  you  that  care  may  be  necessary 
to  distinguish  the  earlier  phases  of  hyperpiesia  from  anxiety 
states,  from  neurasthenia,  and  from  simple  over-work.  A 
small  haemoptysis  with  fatigue  symptoms  may  raise  a 
suspicion  of  pulmonary  tubercle.  When  the  heart  becomes 
enlarged  and  murmurs  develop,  the  differentiation  from 
primary  cardiac  disease  must  also  be  made.  Of  all  the  causes 
of  organic  heart-disease  hyperpiesia  is  the  commonest.  In  a 
patient  of  middle  age  with  no  previous  history  of  rheumatic 
or  syphilitic  infection,  the  development  of  cardiac  symptoms 


HYPERPIESIA  SIC 

or  signs  should  be  an  immediate  signal  for  blood -pressure 
observations. 


Prognosis1 

Enough  lias  already  been  said  to  show  you  that  prognosis 
is  difficult  in  the  early  or  middle  periods  of  the  disease;  but 
when  serious  vascular  lesions  or  cardiac  failure  develop,  the 
outlook  is  obviously  bad.  With  the  slighter  symptoms  and 
objective  signs  of  cardiac  involvement  or  repeated  small 
vascular  lesions  the  forecast  must  needs  be  guarded.  If,  how- 
ever, the  case  be  seen  in  the  early  stage,  when  symptoms 
rather  than  signs  give  the  clue  to  the  diagnosis,  and  if  a 
suitable  way  of  life  can  be  enjoined,  the  outlook  may  be 
quite  good,  although  longevity  is  not  probable.  A high 
blood-pressure  discovered  independently  of  other  symptoms 
or  signs  of  hyperpicsia  in  the  course  of  a routine  examina- 
tion should  be  confirmed  by  further  observations,  and  does 
not  necessarily  demand  a gloomy  forecast.  A very  high 
diastolic  pressure  is  relatively  of  more  serious  import  than 
a high  systolic  pressure.  A case  occurring  at  the  menopause 
may  sometimes  improve  greatly  when  this  phase  of  life  is 
past.  The  patient’s  fitness  in  other  ways,  his  mode  of  life 
and  his  family  history  must,  of  course,  always  be  taken  into 
account,  for  prognosis,  like  diagnosis,  should  invariably  be 
based  upon  a careful  general  survey.  It  need  hardly  be  added 
that  to  the  patient  himself  as  good  a prognosis  as  possible 
should  be  given,  provided  it  does  not  so  enhance  his  sense 
of  security  as  to  make  him  neglectful  of  his  therapeutic  rules. 

Treatment 

It  might  at  first  seem  hopeless  to  suggest  remedial  measures 
for  so  insidious  and  seemingly  so  relentless  a disease,  but  in 
point  of  fact,  n groat  deal  of  good  may  be  done  in  little  ways, 
Medicines  play  a small  part  only  in  the  treatment.  Nitrites 
should  not  be  prescribed  excepting  for  the  treatment  of  such 
urgent  symptoms  as  anginal  pain.  Iodides  arc  said  to  reduce 
the  pressure  but  are  of  uncertain  value,  and  it  should  probably 
be  our  aim  rather  to  check  or  delay  the  further  rise  of  pressure 

1 Vide  also  Chapter  XX. 


314  HYPERPIESIA 

than  to  produce  a fall.  A restful  life,  where  possible,  with 
avoidance  of  physical  and  still  more  of  mental  fatigue; 
avoidance  of  hurry,  worry,  and  flurry;  a dietary  regime 
tending,  but  not  too  strictly,  towards  the  vegetarian;  good 
holidays;  and  reassurance  and  bromides  for  the  anxious- 
minded  patients,  all  play  their  part.  The  consumption  of 
tobacco  and  alcohol  should  be  kept  witliin  reasonable  limits, 
and  the  latter,  if  previously  taken  to  excess,  forbidden. 
Weight  reduction  in  obese  cases  is  valuable,  and  produces 
more  subjective  and  objective  improvement  than  any  other 
single  measure.  Never  tell  the  patient  his  actual  blood- 
pressure  readings.  Periodic  venesections  in  the  plethoric 
type  of  hyperpietic  patient  have  been  recommended,  in  the 
old  days  were  much  practised,  and  would  seem  rational,  but 
the  results  arc  not  lasting.  With  hyperpiesia,  ns  with  every 
other  disease,  early  diagnosis  is  the  most  important  hand- 
maid of  treatment.  I would  therefore  urge  you  to  familiarize 
yourselves  with  subjective  symptoms,  however  trivial,  and 
always  to  try  to  find  for  them  a rcasonnl  interpretation.  You 
should  also  practise  your  fingers,  your  stethoscopes,  and 
your  ophthalmoscopes  assiduously.  Examine  all  radial 
arteries  with  care,  and  register  the  systolic  and  diastolic 
blood-pressure  with  the  sphygmomanometer  in  every  case 
in  which  it  falls  to  you  to  perform  a routine  overhaul.  The 
forefinger  may  readily  learn  to  judge  the  presence  of  very 
high  and  very  low  pressures,  but  with  figures  between  110 
170  mm.  of  mercury  it  is  impossible  to  be  accurate. 

Finally,  for  its  historical  value  and  associations,  it  is  of 
interest  to  consult  an  article  entitled  ‘Some  of  the  Clinical 
Aspects  of  Chronic  Bright’s  Disease’,  in  the  Guy's  Ilospilal 
Reports  for  1879,  by  Dr.  Mahomed,  then  Medical  Registrar, 
and  later  Assistant  Physician  to  Guy’s  Hospital.  Without 
the  aid  of  the  sphygmomanometer,  which  was  not  then 
invented,  but  with  the  aid  of  the  sphygmograph.  Dr.  Maho- 
med was  among  the  first  to  throw  light  upon  the  importance 
of  blood-pressure  observations  in  disease,  and  to  predict 
much  that  has  since  been  established  in  regard  to  this 
interesting  and  prevalent  malady. 


xxm 


‘CHRONIC  BRIGHT’S  DISEASE  WITHOUT 
ALBUMINURIA’1 

AN  inSTORICAL  NOTE  ON  THE  CONTRIBUTIONS  OF 
BRIGHT  AND  HIS  SUCCESSORS  OF  TIIE  GUY’S  SCHOOL 
TO  TIIE  STUDY  OF  HIGH  BLOOD-PRESSURE  AND  ITS 
CONSEQUENCES 

It  is  clear  from  a perusal  of  Bright’s  writings  on  the  disease 
which  bears  his  name,  and  notably  from  a study  of  the  cases 
included  in  his  ‘Tabular  View  of  the  Morbid  Appearances 
in  100  Cases  connected  with  Albuminous  Urine’,2  that  his 
descriptions  were  concerned  with  several  varieties  of  renal 
damage.  This  he  undoubtedly  appreciated  himself,  but  for 
the  most  part  he  was  content  to  record  his  observations 
upon  them  and  refrained  from  advancing  theories  of  their 
relationships  and  origins.  Gradually  others  who  followed 
him,  and  not  least  among  these  certain  physicians  of  the 
Guy’s  school,  helped  to  differentiate,  both  anatomically  and 
clinically,  the  several  forms  of  ‘morbus  Brightii’. 

The  form  of  the  disease  with  which  this  note  is  concerned 
is  that  which  has  now  come  to  be  regarded  (largely  tlirough 
the  researches  of  Wilks,  Gull,  and  Mahomed)  as  primarily  a 
disease  of  the  arterioles  and  capillaries  and  only  secondarily 
of  the  kidneys.  In  this  disease  the  most  outstanding  and 
constant  clinical  feature  is  an  excessive  rise  in  the  arterial 
blood -pressure;  the  most  outstanding  pathological  features 
are  the  presence  of  certain  changes  in  the  vessels,  originally 
described  by  Gull  as  ‘ nrtcrio-capillary  fibrosis’,  and  of 
cardiac  hypertrophy.  In  Bright’s  ‘Tabular  View'  there  are 
records  of  several  patients  in  the  middle  period  of  life  who 
are  shown  to  have  succumbed  to  cerebral  haemorrhage  or 
heart  failure,  and  in  whose  post-mortem  findings  are  re- 
ported kidneys  ‘small,  hard  and  granulated’,  and  hearts 
showing  ‘great  hypertrophy  of  the  left  ventricle’.  These 

1 Guy’*  Hospital  Tlrports  (Bright  Centenary  Number),  1027,  Ixxvil.  307. 

* Guy't  Hospital  Hfportt,  1830. 1.  3S0. 


31 C CHRONIC  BRIGHT’S  DISEASE 

cases  were  evidently  distinct  from  those  in  which  death 
occurred,  usually  at  an  earlier  age,  with  anasarca  or  uraemia, 
and  (employing  the  modem  clinical  terminolgy  suggested 
by  Sir  Clifford  Allbutt)  may  be  accepted  as  examples  of 
‘hyperpiesia*  in  its  latest  stage. 

The  story  of  high  blood-pressure  and  its  consequences 
may  therefore  be  said  to  have  started  with  the  final  chapter, 
for  Bright  concerned  himself  almost  entirely  with  its  morbid 
anatomy  and  terminal  morbid  physiology.  He  was  only 
indirectly  responsible  for  the  chapters  added  later  by  others 
working  under  the  inspiration  of  his  pioneer  studies.  Never- 
theless, while  principally  concerned  with  the  demonstration 
of  the  renal  changes  and  of  the  frequent  association  of  albu- 
minuria, Bright  was  very  much  alive  to  the  coincidence  of 
damage  in  other  organs,  and  especially  in  ‘the  circulating 
system*.  The  cardiac  hypertrophy  attracted  his  attention, 
and  the  hard  pulse,  which  had  long  been  a familiar  accom- 
paniment of  apoplexy,  became  associated  at  this  time  with 
the  more  general  pathological  picture  which  he  painted.  In 
so  far  as  he  allowed  himself  to  consider  causes  Bright  wrote 
with  customary  caution,  and  while  naturally  inclined,  in  the 
light  of  his  discovery,  to  regard  the  kidney  as  prime  offender, 
he  was  far-seeing  enough  to  remark,  * . . . yet  we  are  not  at 
liberty  to  assume  that  the  disease  of  the  kidney  has  been 
the  primary  cause  on  which  the  disease  of  the  rest  depended*. 
When  discussing  the  structural  changes  in  the  heart  he  is 
equally  guarded,  and,  commenting  upon  the  frequency  of 
hypertrophy  without  valvular  disease,  he  continues:  ‘This 
naturally  leads  us  to  look  for  some  less  local  cause  for  the 
unusual  efforts  to  which  the  heart  has  been  impelled ; and 
the  two  most  ready  solutions  appear  to  be,  either  that  the 
altered  quality  of  the  blood  affords  irregular  and  unwonted 
stimulus  to  the  organ  immediately ; or,  that  it  so  affects  the 
minute  and  capillary  circulation  as  to  render  greater  action 
necessary  to  force  the  blood  tlirough  the  distant  subdivisions 
of  the  vascular  system.  * 

Beyond  these  observations  and  opinions  we  can  trace 
little  in  Bright’s  papers  which  seems  to  have  a direct  bearing 
on  the  problem  of  arterial  disease  and  high  blood-pressure, 


WITHOUT  ALBUMINURIA  817 

but  when  we  consider  that  his  researches  formed  the  ground- 
work upon  which  the  investigations  of  Wilks,  of  Gull  and 
Sutton,  and  of  Mahomed  were  founded,  they  assume  an 
additional  importance  and  remind  us  that  * morbus  Brightu’ 
was  a discovery  which  cast  its  illumination  over  far  more 
than  the  renal  tubules  and  added  not  one  but  several  new 
chapters  to  the  book  of  medical  knowledge. 

Reviewing  the  writings  of  those  who  followed  him,  it 
would  seem  that,  for  more  than  fifty  years  after  his  last 
publications  on  renal  disease  and  albuminuria,  chronic 
Bright’s  disease  was  held  especially  to  imply  that  malady 
of  middle  life  which  clinicians  of  a later  generation  have 
labelled  variously  ns  arteriosclerosis  or  hyperpiesia,  and 
pathologists  os  artcrio-capillary  fibrosis,  arteriosclerosis,  or, 
more  recently,  diffuse  hyperplastic  sclerosis.  In  the  earlier 
stages  of  its  history  that  form  of  the  disease  which  we  now 
call  ‘chronic  interstitial  nephritis*  was  apparently  not 
separately  identified. 

In  1852  Sir  Samuel  (then  Doctor)  Wilks  contributed  a 
long  article  to  the  Reports,  entitled  ‘Cases  of  Bright’s 
Disease,  with  Remarks’.1  He  notes  that  albuminuria  is 
not  invariably  a symptom  of  chronic  Bright’s  disease,  and 
vividly  contrasts  a case  of  acute  dropsical  disease  in  a young 
woman  presenting  large  white  kidneys  at  autopsy,  with  an 
almost  symptomicss  case  of  sudden  death  in  an  old  man 
whose  kidneys  were  found  to  be  small  and  red  and  hard. 
Several  of  the  descriptions  in  the  appended  list  of  83  cases 
belonging  to  this  second  group  refer  to  examples  of  ‘liyper- 
picsia*  with  death  by  ‘cardiac  defeat’  (Clifford  Allbutt) 
or  by  cerebral  haemorrhage.  Wilks  also  comments  upon 
the  variety  of  complaints  with  which  sufferers  from  chronic 
Bright’s  disease  present  themselves,  none  of  them  neces- 
sarily incriminating  the  kidney,  and  remarks  that  ‘ the  con- 
dition of  the  artery  on  feeling  the  pulse  often  leads  to  the 
suspicion  of  the  disease,  a thickened  tortuous  artery  occur- 
ring so  frequently  in  “morbus  Brightii”’.  Furthermore,  in 
respect  of  the  findings  after  death,  he  is  struck  by  the  in- 
variable presence  of  arterial  disease  in  those  cases  which 
1 Guy’*  Ilatpilzl  R/porti  (2rul  Series),  1 832,  111.  252. 


318  CHRONIC  BRIGHT’S  DISEASE 

show  cardiac  hypertrophy.  Beyond  hinting  at  the  possible 
influence  of  senescence  and  alcoholism  and  discountenanc- 
ing the  influence  of  gout  and  scrofula  he  has  little  to  suggest 
in  respect  of  aetiology. 

Twenty  years  later  Sir  William  Gull,  writing  in  conjunc- 
tion with  Dr.  H.  G.  Sutton,  gave  to  the  world  his  classical 
account  of  ‘ The  Pathology  of  the  Morbid  State  commonly 
called  Chronic  Bright’s  Disease  with  Contracted  Kidney*.1 
As  the  result  of  careful  anatomical  and  histological  re- 
searches he  established  the  disease  for  the  first  time  as  one 
of  the  arteries  and  capillaries,  and  stated  his  conclusions  as 
follows: 

‘(1)  There  is  a diseased  state  cliarncterizcd  by  hyaline-fibroid  for- 
mation in  the  arterioles  and  capillaries. 

‘(2)  This  morbid  change  is  attended  with  atrophy  of  the  adjacent 
tissues. 

‘(3)  It  is  probable  that  this  morbid  change  commonly  begins  in  the 
Iddney,  but  there  is  evidence  of  its  also  beginning  primarily  in  other 
organs. 

'(4)  The  contraction  and  atrophy  of  the  kidney  are  but  part  and 
parcel  of  the  general  morbid  cliange. 

‘(5)  The  kidneys  may  be  but  little  if  at  all  affected,  whilst  the 
morbid  change  is  far  advanced  in  other  organs. 

‘(6)  This  morbid  change  in  the  arterioles  and  capillaries  is  the 
primary  and  essentia!  condition  of  the  morbid  state  called  chronic 
Bright’s  disease  with  contracted  kidney. 

‘(7)  The  clinical  history  varies  according  to  the  organs  primarily 
and  chiefly  affected. 

*(8)  In  the  present  state  of  our  knowledge  we  cannot  refer  the 
vascular  changes  to  an  antecedent  change  in  the  blood  due  to  the 
defective  renal  excretion. 

*(9)  The  kidneys  may  undergo  extreme  degenerative  changes 
without  being  attended  by  the  cardiovascular  and  other  lesions 
characteristic  of  the  condition  known  as  chronic  Bright’s  disease. 

*(10)  The  morbid  state  under  discussion  is  allied  with  the  condi- 
tions of  old  age,  and  its  area  may  be  said  hypothetically  to  corre- 
spond to  the  “area  vasculosn”. 

*(11)  The  changes,  though  allied  with  senile  alterations,  are  prob- 
ably due  to  distinct  causes  not  yet  ascertained. 

‘Should  it  be  considered  necessary  to  distinguish  this  morbid  state 
by  any  special  term,  we  venture  to  suggest  for  the  purpose  the  name 
“arterio-capillary  fibrosis’’.* 

1 3 ledico-Chirurgical  Transactions,  1872,  Iv.  273. 


WITHOUT  ALBUMINURIA  310 

Gull  goes  farther  than  Wilks,  who  found  that  albumin 
was  not  necessarily  present  in  the  urine,  for  he  shows  that 
the  kidneys  themselves  may  show  no  gross  changes.  The 
sufferers  from  the  disease  he  finds,  as  has  always  been 
remarked,  principally  at  or  after  middle  life  and  very  rarely 
in  youth.  Ever  insistent  on  the  importance  of  ‘ the  general 
view’,  he  concludes  a clinical  lecture1 *  on  the  subject  of 
arterio-capillary  fibrosis,  given  at  Guy’s  Hospital,  in  the 
following  dramatic  sentences: 

*It  is  always  dangerous  to  rest  in  a narrow  pathology ; and  I believe 
that  to  be  a narrow  pathology  which  Is  satisfied  with  what  you  now 
see  before  me  on  this  table.  In  this  glass  you  see  a much  liypcrtro- 
phled  heart  and  a very  contracted  kidney.  This  specimen  is  classical. 
It  was,  I believe,  put  up  under  Dr.  Bright’s  own  direction,  and  with 
a view  of  showing  that  the  wasting  of  the  kidney  is  the  cause  of  the 
thickening  of  the  heart.  I cannot  but  look  upon  it  with  veneration, 
hut  not  with  conviction.  I think,  with  all  deference  to  so  great  an 
authority,  that  the  systemic  capillaries,  and,  had  it  been  possible,  the 
entire  man,  should  hove  been  included  in  this  vase,  together  with  the 
heart  and  the  kidneys ; then  w e should  hove  had,  I believe,  a truer 
view  of  the  causation  of  the  cardiac  hypertrophy  and  of  the  disease 
of  the  kidney.’ 

Improvements  in  histological  technique  and  staining 
methods  may  have  modified  or  corrected  their  more  detailed 
opinions,  but  the  general  conception  of  Gull  and  Sutton 
remains  uncontroverted. 

W'c  pass  next  to  a review  of  some  remarkable  contributions 
written  from  the  clinical  standpoint.  I refer  to  the  papers  by 
Dr.  F.  A.  Mahomed  which  appeared  in  various  journals 
between  the  years  1874  and  1881,  and  of  which  the  more 
important  are  to  be  found  in  the  Guy's  Hospital  Reports  for 
the  years  1870"  and  1881.3  From  the  second  of  these,  which 
was  submitted  as  a thesis  for  the  degree  of  M.B.  in  the 
University  of  Cambridge,  I have  borrowed  the  title  of  the 
present  memoir.  The  title  and  the  paper  leave  no  room  for 
doubt  that  Mahomed  was  concerned  with  the  description 
of  what  we  now  call  ‘ hyperpiesia  Sir  Clifford  Allbutt  in 

1 J hit.  Med.  Joum.,  21  Dec.  3 872 

* ‘Some  of  the  Clinical  Aspects  of  Chronic  I! right’s  Disease.* 

* * Cl  ironic  Bright's  Disease  without  Albuminuria.* 


320  CHRONIC  BRIGHTS  DISEASE 

his  work  on  Diseases  of  ike  Arteries  pays  tribute  to  Maho- 
med’s work,  but  I cannot  help  feeling  that  many  other 
writers  on  the  subject  of  high  blood-pressure  have  done  but 
scant  justice  to  his  painstaking  researches.  Mahomed  may 
be  regarded  as  one  of  the  chief  pioneers  of  blood-pressure 
observations  in  disease.  He  had  no  sphygmomanometer 
such  as  we  possess,  but  with  the  aid  of  his  fingers,  his  own 
modification  of  Morey’s  sphygmograph,  and  the  roughest 
methods  of  measuring  pressures,  which  he  expressed  in 
terms  of  ounces,  he  amassed  records  and  marshalled  argu- 
ments which  ore  a monument  to  his  zeal  and  industry  and 
brilliant  intellect.  More  clearly  than  any  one  previously  he 
defined  clinically  that  form  of  Bright’s  disease  which  tends 
to  terminate  with  apoplexy  or  heart -failure.  Having  estab- 
lished what  he  called  a pre-albuminuric  phase  of  the  disease, 
he  then  showed  that  albumin  could  be  absent  in  all  stages, 
and  when  present  terminally  that  this  was  sometimes  on 
effect  rather  of  heart-failure  than  of  renal  damage.  He 
showed  that  in  the  absence  of  albuminuria  the  disease  could 
be  readily  diagnosed  by  observation  of  the  symptoms,  the 
pulse,  and  the  position  of  the  apex  beat,  and  by  careful 
analysis  of  the  type  of  tracing  obtained  with  the  sphygmo- 
graph. He  sought  to  explain  the  various  qualities  of  the 
pulsus  magnus,  durus  et  tardus  of  the  old  physicians  on 
the  basis  of  liis  sphygmographic  findings.  He  accounted 
reasonably  for  many  of  the  symptoms  of  high  blood-pressure 
and  described,  with  much  attention  to  detail,  the  ways  in 
which  the  heart  may  fail.  He  illustrated  graphically  some 
types  of  peculiar  cardiac  rhythm  which  he  encountered 
in  cases  of  heart-failure  due  to  high  arterial  pressure,  em- 
ploying not  only  sphygmographic  records  but  simultaneous 
records  from  the  radial  and  jugular  pulses  and  the  apex 
beat.  He  discussed  the  murmurs  of  heart-failure  in  chronic 
Bright’s  disease  and  showed  that,  while  simulating  the 
murmurs  of  valvular  disease,  they  were  not  due  to  valvular 
lesions,  paying  particular  attention  to  the  presystolic  murmur 
not  infrequently  heard  in  cases  of  pronounced  cardiac  dilata- 
tion. He  pointed  out  that  while  the  ‘red’  contracted  kidney 
could  be  unaccompanied  by  albuminuria,  the  ‘yellow*  or 


without  albuminuiua  a si 

‘mixed’  contracted  kidney  gave  albumin  and  a urine  gene- 
rally of  lower  specific  gravity.  lie  showed  that  in  scarlatina 
the  blood-pressure  rises  before  the  development  of  albumi- 
nuria or  other  evidences  of  nephritis.  lie  put  in  a plea  for  the 
view,  still  maintained  by  many,  that  high  blood-pressure  pre- 
cedes aiid may  cause  artcrio-capillary  fibrosis,  and  argued  that 
the  high  pressure  could  not  be  attributed  solely  to  organic 
arterial  changes,  since  Broadbcnt  had  demonstrated  a 
reduction  of  high  pressure  with  amyl  nitrite,  presumably  by 
arterial  relaxation.  He  insisted  that  high  arterial  tension 
and  not  albuminuria  should  be  accepted  as  the  sign  of  chronic 
Bright’s  disease.  He  emphasized  the  possibility  and  impor- 
tance of  early  diagnosis.  He  found  high  pressures  in  a small 
percentage  of  young  people,  and  discussed  ‘ the  recognition 
of  the  Diathesis  in  young  persons  during  health  and  previous 
to  structural  change’,  and  in  further  support  of  the  influence 
of  constitution  adduced  the  high  incidence  of  apoplexy  in 
some  families.  And  finally,  notwithstanding  the  changes  of 
view  for  which  he  himself  was  partly  responsible,  lie  loyally 
insisted  on  the  retention  of  ‘chronic  Bright’s  disease’  as  the 
most  fitting  nomenclature. 

If  we  except  the  comparatively  small  additions  to  our 
knowledge  which  have  accrued  through  perfected  technical 
and  instrumental  aids — that  is  to  say,  through  the  agency 
of  the  sphygmomanometer,  better  interpretation  of  ophthal- 
moscopic appearances,  improved  histological  methods,  and 
the  arrival  of  new  methods  of  testing  cardiac  and  renal  func- 
tion— we  may,  I believe,  justly  claim  that  the  whole  of  the 
story  of  high  blood-pressure,  including  the  little  we  know  of 
its  aetiology  and  the  great  deal  we  know  of  its  consequences, 
was  written  at  Guy’s  between  the  years  1827  and  1881. 

Other  causes  of  ‘ hj'perpiesis  ’ — physiological  and  emo- 
tional, or  expressing  increased  intracraninl  pressure  or  an 
over-active  thyroid  gland — have  been  revealed,  but  there  is 
only  one  ‘ hyperpiesia,’  and  that  is  chronic  Bright’s  disease 
without  (and  sometimes  with)  albuminuria.  For  the  history 
of  this  disease  Bright,  Wilks,  and  Gull  provided  the  patho- 
logical and  Inter  clinical  chapters,  while  Mahomed  completed 
the  clinical  episode  in  all  its  phases. 

Y 


322  CHRONIC  BRIGHTS  DISEASE 

Of  prime  causes — however  much  we  may  speculate  about 
a ‘pressor  substance’ — we  know  no  more  to-day  than  they 
did ; of  prognosis  and  treatment  very  little  more, 

Bright’s  influence  on  medical  thought  and  teaching  at 
Guy’s  has  made  itself  felt  in  successive  generations  and  in 
various  ways ; partly  through  the  lustre  of  his  name  and 
achievement  and  partly  through  his  initiation,  in  concert 
with  Addison  and  Hodgkin,  of  a famous  line  of  physician- 
pathologists,  with  its  tradition  of  faithful  observation  and 
record  at  the  bedside,  pursued  and  completed,  whenever 
possible,  in  the  post-mortem  room. 

The  purpose  of  this  brief  memoir  has  been  to  indicate  how, 
in  a more  direct  manner,  the  researches  of  Richard  Bright 
provided  a basis  and  inspiration  for  subsequent  investiga- 
tions of  permanent  value,  carried  out  within  the  same  pre- 
cincts and  in  accordance  with  his  own  sound  principles,  on 
the  predominant  variety  of  his  own  disease. 


XXIV 

ANGINA  PECTORIS  AND  ALLIED  SEIZURES1 

In  the  list  of  diseases  with  which  wc  go  armed  in  practice 
there  are  a few  which  stand  apart  by  reason  of  some  peculiar 
interest  or  importance  attaching  to  them,  or  of  the  urgency 
of  the  situations  which  they  create.  Of  such  are  typhoid 
fever,  syphilis,  pneumonia,  and  the  abdominal  emergencies, 
but  none,  perhaps,  make  a stronger  appeal  to  the  mind  than 
those  cardiovascular  disorders  which  have  as  their  major 
manifestation  the  dreaded  breast-pang.  Since  Ueberden,  in 
1708,  painted  for  us  with  simple,  vivid  plirnsc  the  clinical 
picture  of  angina  pectoris,  it  has  always  claimed  the  atten- 
tion and  stirred  the  curiosity  of  physicians.  The  reasons  nre 
not  far  to  seek.  A fully  developed  anginal  attack,  even  in 
the  narrative,  and  how  much  more  in  the  witnessed  event, 
is  a drama  in  itself,  and,  all  too  often,  prophetic  of  human 
tragedy.  On  the  academic  side  we  arc  faced  with  the  ever- 
present difficulties  of  explaining  the  phenomena  and  fore- 
casting the  issue  of  the  attacks,  which  frequently  arrive  in 
the  midst  of  apparent  health  and  in  the  absence  of  gross 
evidences  of  disease.  For  these  reasons,  and  because  pain 
has  always  seemed  to  me  to  be  one  of  the  most  necessary 
and  fascinating  studies  open  to  the  practising  part  of  our 
profession,  I decided  that  the  pain  of  pains,  and  some  of  its 
near  congeners,  would  make  a fitting  topic  for  discussion. 
I shall  confine  myself  to  a consideration  of — 

1.  The  clinical  features  of  the  anginal  syndrome. 

2.  Its  clinical  varieties  and  their  significance  (forit  is  most 
important  not  to  regard  angina  as  expressive  of  any 
single  pathology). 

3.  Some  other  conditions  which  bear  a close  resemblance 
to  it. 

By  my  descriptions  I shall  endeavour  to  suggest  some 
working  views  in  respect  of  the  classification  of  cases,  the 

• ClimVnI  Journo?,  1027,  IvL  CIS. 


324  ANGINA  PECTOIIIS  AND  ALLIED  SEIZURES 
nature  of  the  symptoms,  and  the  prognosis  in  the  several 
disorders  of  which  these  symptoms  are  eloquent. 

Aetiology  and  Pathology 

In  regard  to  aetiology  and  pathology  let  it  suffice  to  say 
that  angina  pectoris,  taking  the  graver  forms,  occurs  mostly 
at  or  after  the  nge  of  50,  and  that  it  is  much  more  common 
in  men  than  women ; but  that,  taking  all  forms,  it  may  occur 
at  any  period  of  adult  life  and  is  fairly  evenly  distributed 
between  the  sexes ; that  it  is  frequently — but  not  invariably 
■ — associated  with  changes  in  the  arteries  and  particularly — • 
though  not  necessarily — with  atheroma  of  the  first  part  of 
the  aorta  and  the  coronary  vessels ; that  in  younger  subjects 
it  may  be  associated  with  syphilitic  aortitis;  and  that 
‘nervous’,  ‘anaemic’,  and  ‘toxic’  varieties,  without  demon- 
strable organic  change,  arc  also  encountered.  The  fact  that 
it  has  so  many  and  such  varied  associations  at  once  suggests 
the  impropriety  of  regarding  angina  pectoris  as  a disease.  It 
is  not  a disease  but  a syndrome  (or  group  of  symptoms), 
and  yet  such  a dramatic  syndrome  that  it  assumes  the  impor- 
tance of  a disease  in  our  minds. 

The  Pain 

Now'  the  main  symptom  is  indubitably  the  pain,  and  it 
is  a pain  of  such  a peculiar  kind  and  often  of  such  severity 
that  it  merits  special  study.  It  will  be  generally  conceded 
that  the  pains  of  visceral  disease  in  which  physical  signs 
are  scanty  or  altogether  lacking  require  a more  searching 
analysis  than  those  with  clear  objective  associations.  It  is, 

I believe,  a good  plan  to  employ  some  definite  scheme  of 
analysing  such  pains.  I would  suggest  that  our  interroga- 
tor}' should  include  ten  questions  [vide  Lecture  HI).  Of 
these  two  have  reference  to  quality  and  quantity,  and  may 
be  answered  under  the  headings  of  character  and  severity. 
Three  have  reference  to  the  location  or  spacial  relationships 
of  the  pain,  and  may  be  answered  under  the  headings  of  situa- 
tion, localization  (or  extent  of  diffusion),  and  paths  of  refer- 
ence. Three  have  reference  to  temporal  relationships,  and 
maybe  answered  under  the  headings  of  duration,  frequency. 


ANGINA  PECTORIS  AND  ALLIED  SEIZURES  325 
and  particular  times  of  occurrence.  Two  have  reference  lo 
determining  causes,  and  may  be  answered  under  the  headings 
of  aggravating  and  relieving  factors.  Overand  above  all  these 
our  inquiry  must,  of  course,  include  associated  symptoms. 

Let  us  apply  these  questions  in  the  case  of  the  pain  of 
angina  pectoris.  Of  its  character  in  bad  cases  we  might 
almost  say  that  it  defies  description,  but  it  is  generally 
recorded  as  a crushing,  bursting,  constricting,  or  vice-like 
pain.  In  severity  it  varies  from  a mere  sense  of  discomfort  or 
oppression — often  at  first  it  is  mistaken  for  flatulence — to 
the  extremest  agony  that  man  is  called  upon  to  suffer.  Of 
its  situation  we  may  say  that  it  is  generally  retrosternal,  but 
it  may  be  ns  high  as  the  manubrium,  as  low  as  the  ensiform, 
or  even  epigastric.  Sometimes  it  is  situated  to  the  left  and 
lies  within  the  praecordial  zone.  Its  localization  is  fairly  con- 
fined and  accurate,  and  may  be  indicated  with  a closed  fist 
held  against  the  sternum,  but  its  possible  paths  of  reference 
arc  numerous  and  wide.  Most  common  and  characteristic 
is  the  reference  down  the  inner  side  of  the  left  arm  to  the 
elbow,  or  ns  far  ns  the  ring  and  little  fingers  of  the  left  hand ; 
but  it  may  also  pass  into  the  right  arm,  up  the  side  of  the 
neck,  or  into  the  jaw.  The  duration  of  an  anginal  paroxysm, 
induced  as  it  usually  is  by  some  physical  effort,  is  a matter 
of  minutes  rather  than  seconds  or  hours,  but  it  is  common 
for  the  attacks  to  become  more  prolonged  with  the  passage 
of  time.  The  frequency  of  the  paroxysms  is  very  variable.  A 
man  may  die  in  his  first  attack,  or  survive  it  for  many  years 
with  frequent  attacks  or  with  long  freedom  from  pain. 
Generally  speaking,  they  tend  to  become  more  frequent  and 
to  arrive  for  lesser  causes.  Of  particular  times  of  occurrence 
Heberden  is  careful  to  mention  the  early  hours  of  the  morn- 
ing after  the  first  sleep,  when  other  ‘spasmodic  complaints* 
are  habJc  to  assert  themselves.  Of  aggravating  causes,  physi- 
cal efforts  such  ns  walking  up  a slope  (especially  * on  a full 
stomach’},  anger,  anxiety,  and  cold  arc  nil  noteworthy. 
Peace  of  body  and  mind,  warmth,  and,  in  the  attacks,  abso- 
lute immobility  and  amyl  nitrite  are  the  main  relieving 
factors.  Of  associated  symptoms  the  'angor  animi*  is  the 
most  remarkable,  but  only  occurs  in  nbout  20  per  cent,  of 


320  ANGINA  FECTORIS  AND  ALLIED  SEIZURES 
cases.  It  is  sometimes  referred  to  as  ‘the  fear  of  impending 
death*.  More  correctly  it  is  an  actual  ‘sense  of  dying*,  and 
sometimes  more  awful  in  its  effect  upon  the  patient’s  mind 
than  his  physical  sufferings.  A sense  of  restricted  breathing 
(but  without  dyspnoea),  tingling  and  numbness  (instead  of 
pain)  in  the  arms,  and  polyuria  after  the  attack  may  also  be 
mentioned.  Between  attacks  the  patient  at  first  feels  well 
and  may  appear  to  be  in  robust  health.  Should  heart-failure 
with  nirhythmia  or  congestive  signs  supervene  the  attacks 
may  altogether  disappear.  Summarizing  the  features  of  the 
anginal  seizure  in  a single  brief  definition,  we  may  say  that 
it  is  * a substcrnal  pain  of  cardiovascular  origin,  paroxysmal 
in  character,  sometimes  of  great  severity,  most  constantly 
induced  by  effort  and  relieved  by  rest,  and  in  some  cases  asso- 
ciated with  a peculiar  sense  of  dying \ ‘Heart-attacks  ’ with- 
out pain  and  not  conforming  in  some  of  the  main  particulars 
with  this  description  cannot  be  certainly  regarded  os  anginal, 
and  when  we  come  to  consider  the  peripheral  * allied  seizures’, 
these,  too,  should  show  analogous  characters. 

The  Clinical  Vakieties 

I would  next  ask  your  consideration  of  the  clinical  varieties 
of  angina  pectoris,  and  in  this  I may  perhaps  best  help  by 
selections  from  my  case-notes,  so  arranged  as  to  give  pic- 
tures, first  of  the  more  innocent,  then  of  the  less  innocent, 
and  finally  of  the  gravest  forms.  At  this  point,  too,  I would 
ask  you  to  decide  whether  we  should  continue  to  employ 
or  finally  reject  the  term  ‘pseudo-angina*.  I would  plead 
for  its  rejection,  or  for  its  retention  only  as  an  instrument 
for  reassuring  an  anxious  patient  afflicted  with  what  lie  or 
she  has  regarded  as  a grave,  but  what  we  believe  to  be  an 
innocent,  angina.  It  may  be  true  that  the  more  innocent 
forms  are  commoner  in  women,  and  occur  at  an  earlier  age ; 
but  if  the  symptoms  have  a genuine  relationship  to  those 
included  in  our  definition  they  are  surely  * anginal  When  a 
patient  has  hunger-pain  from  excessive  smoking  or  worry, 
we  do  not  say  that  he  has  pseudo-hunger-pain  because  he 
lacks  a duodenal  ulcer.  Surely  it  were  better  to  speak  of 
benign  and  malign  angina  rather  than  of  false  and  true 


ANGINA  FECTORIS  AND  ALLIED  SEIZURES  327 
angina,  for,  from  a practical  point  of  view,  what  we  have 
to  decide  in  the  individual  case  is — ‘Is  this  a form  of  disease 
about  which  I can  give  a reassuring  prognosis,  or  is  it  one 
which  mny  sooner  or  later  cause  the  patient’s  death  ? ’ 

Before  discussing  even  the  most  innocent  clinical  variety 
of  anginal  seizure  let  us  ask  ourselves — and  it  is  a useful 
question  to  ask  of  any  subjective  symptom — whether  there 
is  anything  in  health  closely  or  remotely  akin  to  it.  I think 
there  is.  Confronted  one  day  at  my  Out-Patients  by  an 
elderly  man  with  a history  of  severe  anginal  attacks,  I asked 
him  to  give  us  as  clear  an  account  as  lie  could  of  what  the 
symptoms  were  like.  His  reply  was:  ‘Well,  sir,  you  know 
as  a young  man  what  it  felt  like  when  you  tried  to  run  a race 
untrained — the  awful,  tight,  bursting  feeling  in  your  chest. 
It  is  like  that,  but  a hundred  times  worse.*  That  was  a good 
observation,  and  you  will  note  that  it  was  the  tight,  bursting 
sensation  and  not  the  dyspnoea  to  which  lie  referred.  The 
anginal  distress,  or  something  akin  to  it,  can  be  evoked  by  a 
supernormal  effort  in  a healthy  person;  in  an  unhealthy 
person  it  may  he  evoked,  and  with  magnified  intensity,  by 
a slight  effort. 

Cask  1.  I was  consulted  for  a transient  dry  pleurisy  by  a healthy- 
looking  woman,  aged  30.  After  describing  licr  present  symptoms  she 
mentioned  quite  casually  that  for  as  long  as  she  could  remember, 
whenever  she  went  out  for  a wnlk  on  a cold  day  she  had  had  a pain 
in  the  chest  which  radiated  down  the  left  arm.  In  every  other  way 
she  was  perfectly  well,  and  she  led  an  active  life.  There  were  no  signs 
of  cardiovascular  disease.  There  was  clearly  no  anxiety  about  her 
case,  and  yet  her  vasomotor  responses  to  cold  combined  with  effort 
were  adequate  for  the  production  of  minor  anginal  pain  with  n typical 
reference. 

Case  2.  A woman,  something  under  40,  came  on  account  of  several 
attacks  within  n period  of  0 months,  characterized  by  a severe  pain 
behind  the  sternum,  radiating  down  the  left  arm  to  the  little  finger, 
which  remained  numb  when  the  attacks  had  passed.  She  also  liad  a 
feeling  as  though  she  were  going  to  die.  The  attacks  generally  came 
on  when  she  was  tired.  She  was  'run  down*  and  unfit,  had  suffered 
a great  emotional  stress,  and  was  working  too  hard.  She  had  liad 
some  minor  rheumatic  symptoms,  but  there  were  no  sign*  of  organic 
disease  of  tire  heart  or  arteries,  and  her  blood  gave  a negative  Waswr- 
mann  test.  With  rest  and  reassurance  she  steadily  improved.  I 


328  ANGINA  PECTORIS  AND  ALLIED  SEIZURES 
regarded  hers  as  a case  of  benSgn  angina  dependent  on  vasomotor 
disturbances  and  not  on  structural  cardioi oscular  disease. 

Case  3.  It  was  less  easy,  although  I elected  to  do  so,  to  give  a 
reassuring  verdict  in  the  case  of  a woman,  aged  52,  who  complained 
of  a pain  behind  the  lower  sternum  induced  by  walking  up  hills,  or 
against  the  wind,  or  by  6uddcn  cold,  or  by  stooping.  The  pain  was 
always  relieved  when  she  stood  still.  It  frequently  radiated  to  the 
left  wrist.  In  every  other  respect  she  felt  perfectly  well.  The  impor- 
tant additional  piece  of  evidence  was  that  she  had  had  the  symptom 
Jot  17  years.  It  developed  at  a time  or  great  mental  anxiety,  when 
a domestic  disruption  lmd  necessitated  her  taking  upon  herself 
physical  and  mental  burdens  and  responsibilities  beyond  what  should 
be  expected  of  any  woman.  To  make  prognosis  still  more  difficult  she 
had  a blood-pressure  of  150  systolic,  00  diastolic,  and  possibly  slight 
hypertrophy  of  the  left  ventricle.  What  were  the  chances  of  her 
benign  angina  becoming  malign  with  the  development  of  organic 
arterial  changes  as  her  age  advanced  ? 

Case  4.  In  the  next  case,  more  typical  of  Heberden’s  description, 
the  prognosis  was  clearly  bad.  A man  of  magnificent  physique,  aged 
07,  complained  or  a gripping  pain  behind  the  lower  sternum  on 
mounting  hills  or  stooping  and  after  food.  It  had  also  caught  him  on 
getting  into  bed— probably  through  the  contact  of  the  cold  sheets — 
and  had  occasionally  wakened  him  at  2 a.m.  It  passed  down  both 
arms  to  the  elbows.  In  a minor  form  he  had  been  occasionally  aware 
of  it  for  5 years.  His  blood-pressure  was  205  systolic,  110  diastolic, 
and  his  urine  showed  a trace  of  albumin.  The  attacks  were  becoming 
more  severe  and  frequent. 

The  severity  or  slightness  of  the  pain  is,  however,  of  no 
certain  prognostic  import. 

Case  5.  An  old  clergyman  who  liad  Jed  a healthy  and  active  life 
complained  of  a ‘bursting’  feeling  behind  the  sternum,  always  in- 
duced by  walking  and  associated  with  tingling  in  the  left  arm.  There 
was  no  agony  and  no  angor  animi.  His  radial  artery  was  slightly 
thickened;  Ins  blood-pressure  was  180  systolic,  110  diastolic;  Ills 
apex  beat  was  in  the  nipple  line;  he  had  frequent  extra-systoles.  He 
was  ordered  rest  and  a prolonged  holiday  from  liis  work.  I saw  him 
again  a few  months  later.  His  signs  were  as  before.  He  reported 
Iximself  as  distinctly  better.  I ventured  to  display  a little  optimism, 
but  did  not  sanction  a resumption  of  duties.  Two  days  l3tcr  he  was 
sitting  still  reading  a book  when  he  fell  hack  dead. 

The  presence  of  any  physical  sign  of  organic  cardiac  change 
in  association  with  angina  calls  for  a guarded  verdict. 


ANGINA  PECTORIS  AND  ALLIED  SEIZURES  320 


Status  Anginosus 

Of  the  ‘allied  seizures’,  the  first  to  be  discussed  is  the  con- 
dition usually  called  ‘status  nnginosus’,  in  which  the  sternal 
or  praecordial  pain  continues  with  great  intensity,  or  is 
repeated  again  and  again  at  short  intervals ; in  which  nitrites 
fail  to  bring  relief,  and  even  heavy  doses  of  morphine  may 
be  only  partially  successful.  This  terrible  condition  is  now- 
shown  to  be  caused  in  almost  every  case  by  coronary  throm- 
bosis with  local  ischaemia  of  the  heart-muscle.  With  it  there 
may  be  slight  fever  for  a few  days  and  a transient  Icueocytosrs. 
The  pain  is  sometimes  referred  to  the  epigastrium,  and,  with 
the  associated  grey  pallor  and  collapse,  may  be  so  strikingly 
suggestive  of  a perforated  ulcer  as  to  lead  to  operation. 
Within  a few  hours  or  days  symptoms  of  heart  failure  may 
supervene  with  congestive  signs;  the  blood -pressure  falls;  the 
heart-sounds  become  distant  and  faint;  occasionally  a fleeting 
pericardial  rub  is  heard.  The  patient  may  die  w-ithin  minutes, 
hours,  or  days  of  the  first  onset,  or  lie  may  recover  with  a 
crippled,  or  a healed  and  apparently  healthy  heart.  Some 
patients  arc  able  to  return  to  their  normal  occupations.  An 
electrocardiogram  usually  reveals  evidence  of  the  myocardial 
damage.  Whilcinsomccascsthcgravitynndlongcontinunncc 
of  the  pain  arc  terrible  to  witness,  in  others  the  gravity  of 
the  attack  is  less  apparent,  or  in  the  place  of  continuous  pain 
there  may  be  brief  recurring  anginal  attacks  at  rest.  Several 
patients,  giving  a typical  history  of  nn  attack,  have  been 
referred  to  me  as  cases  of ' bad  indigestion  \ In  these  physical 
signs  may  be  inconspicuous  or  lacking,  but  the  electrocardio- 
gram may  benr  witness  to  the  presence  of  muscle  damage. 
After  the  acute  phase  patients  may  be  troubled  with  neural- 
gic pains  in  the  back  of  the  neck  and  occiput.  On  returning 
to  active  life  the  angina  of  cfTort  or  dyspnoea  may  be  noted 
for  the  first  time. 

Perusing  the  clinical  accounts  of  cases  of  angina  pectoris 
by  such  great  masters  as  I^ithnm,  Osier,  Clifford  Allbutt, 
and  Mackenzie  we  arc  now  nblc  to  pick  out  with  some  con- 
fidence, from  their  descriptions  alone,  examples  of  nngirta 
which  must  have  l>ccn  due  to  coronary  occlusion.  Turning 


330  ANGINA  PECTORIS  AND  ALLIED  SEIZURES 
to  our  old  case-notes,  we  also  find  descriptions  which  enable 
us  to  separate  this  variety  from  the  general  group  of  anginas. 
Out  of  curiosity  I have  recently  looked  up  the  accounts  of 
John  Hunter’s  illnesses  j1  from  these  it  is  clear  that  his  first 
anginal  seizure  was  in  all  probability  due  to  a coronary 
thrombosis,  and  at  necropsy  20  years  later  typical  scars 
were  found  in  his  heart.  Any  prolonged  anginal  attack  should 
suggest  the  possibility  of  a coronary  thrombosis. 

Anaemic  Angina 

Severe  anaemias  may  cause  angina  of  cTfort  and  can  be 
completely  relieved  by  successful  treatment  of  the  anaemia. 

Case  0.  A successful  business  man,  aged  59,  had  lost  something 
of  his  customary  fitness  after  a period  of  stress  and  worry,  and  then 
had  all  his  teeth  extracted.  Short  1}'  afterwards  he  developed  attacks 
of  angina  pectoris,  especially  when  milking  after  meals.  It  then  be- 
came apparent  that  he  was  losing  weight  and  colour.  Vomiting  was 
an  additional  symptom.  I noted  him  as  of  broad  build  and  short* 
chested.  lie  was  very  obviously  anaemic.  Ilis  tongue  was  sore. 
Heart  not  enlarged.  A soft  systolic  murmur.  B.-P.  120/85.  His 
haemoglobin  was  GO  per  cent,  and  his  blood-picturc  typical  of  per- 
nicious anaemia.  lie  was  treated  with  liver  extract.  In  the  next  8 
months  his  weight  rose  from  10  st.  0 lb.  to  12  st.  0 lb.,  and  he  lost  all 
liis  general  symptoms ; he  no  longer  experienced  anginal  pain,  and 
again  led  an  active  life. 

Vasovagal  Attacks 

There  is  a type  of  vasomotor  storm,  beautifully  described 
by  Gowers  in  his  ‘Borderland  of  Epilepsy’  under  the  head- 
ing of  vasovagal  attacks,  which  may  cause  confusion  and  lead 
to  a diagnosis  of  angina.  In  my  own  experience  these  seizures 
have  always  occurred  in  the  victims  of  anxiety,  usually 
combined  with  slight  general  physical  ill-health;  they 
have  been  rather  more  common  in  women.  The  leading 
symptom  is  wot  pom,  but  ‘the  sense  of  dying*.  The  attacks 
are  not  as  a rule  related  to  physical  effort.  Pain  may  be 
altogether  absent,  or  where  present  amounts  to  a sense  of 
constriction  with  a curiously  frequent  mention  of  a * tugging, 
pain  up  the  left  side  of  the  neck’.  Other  vasomotor  pheno- 
1 See  Lecture  XXV. 


ANGINA  PECTORIS  AND  ALLIED  SEIZURES  33i 
mcna  arc  present,  and  curious  sensations  ore  referred  to  other 
viscera.  The  pulse  may  l>e  quick  or  very  slow  in  the  attacks, 
which  last  minutes  or  an  hour  or  more,  and  are  followed  by 
feelings  of  prostration.  To  the  best  of  my  knowledge  these 
seizures,  however  alarming,  never  kill. 

Abdominal  Angina 

What  else  may  we  include  within  the  category  of  ‘allied 
seizures’?  Firstly,  there  is  abdominal  angina  in  which  (as 
distinct  from  the  epigastric  form  of  angina  pectoris)  the  pain 
is  felt  at  or  below  the  umbilical  level. 

Case  7.  An  ex-sailor,  aged  SO,  with  syphilitic  aortitis  and  aortic 
regurgitation,  complained  of  ‘terrific’  pain  felt  just  below  the  navel, 
coming  aiways  ns  the  result  of  effort,  and  usually  of  very  slight 
effort,  such  os  getting  out  of  bed  or  even  turning  over  in  bed.  There 
was  tenderness  along  the  course  of  the  nbdomlnal  aorta,  but  no  sign 
of  aneurysm. 

Amyl  nitrite  may  bring  relief  in  these  cases. 

We  may  also  meet  with  benign  nbdominnl  angina. 

Cask  8.  A woman  was  Rent  to  my  Out-Patients  ns  a gastric  ease. 
On  inquiry  her  symptom  was  found  to  be  a central  abdominal  pain 
induced  by  walking  and  cased  when  she  6at  down.  She  liad  a throb- 
bing abdominal  aorta  and  definite,  though  slight,  signs  of  hyper* 
thyroidism,  and  was  clearly  a nervous  subject. 

‘Status  anginosus  abdominis’  also  occurs,  and  may  lead 
to  a diagnosis  of  acute  abdominal  disease. 

Case  0.  Recently  I performed  a necropsy  on  a woman  who  died 
ft*  the  result  of  an  attack  of  what  might  well  be  thus  designated.  She 
had  been  admitted  to  a surgical  ward  as  an  acute  obdominal  emer- 
gency, collapsed  and  pale,  and  in  great  pain.  An  exploratory  laparo- 
tomy failed  to  reveal  any  perforated  viscus  or  adequate  cause  for  her 
symptoms.  She  did  not  long  survive.  Before  starting  the  necropsy 
1 discussed  the  possibility  of  coronary  thrombosis.  \Vc  found  ad- 
vanced syphilitic  disease  of  the  abdominal  aorta,  and  the  coeliae  nxfs 
and  right  renal  artery  were  plugged  with  recent  thrombus. 

Angina  Cnuius 

Angina  may  also  occur  in  the  leg.  I prefer  the  title  of 
‘angina  cruris*  to  ‘intermittent  claudication  (or  limping)’, 
which  is  Uic  term  usually  employed  to  describe  a severe  type 


332  ANGINA  PECTORIS  AND  ALLIED  SEIZURES 
of  painful  seizure  affecting  the  leg  in  patients  with  arterial 
disease.  This  pain  is  characteristically  induced  by  walking 
and  relieved  on  standing  still.  Occasionally,  however,  the 
pains,  like  those  of  angina  pectoris,  may  develop  at  rest,  and 
they  may  even  be  accompanied  by  angor  animi.  Further- 
more, angina  pectoris  and  angina  cruris  are  not  infrequently 
recorded  in  the  same  patient. 

Case  10.  An  elderly  male  had  long  had  pain  on  walking.  On  one 
occasion  he  was  seized  with  violent  pain  in  the  leg  while  sitting  at 
his  fireside.  He  to  carried  to  bed  and  passed  a night  of  physical 
and  mental  anguish.  With  evident  awe  he  described  a feeling  during 
the  attack  ‘as  though  his  number  was  up’. 

Benign  cases  of  angina  cruris  with  recovery  have  also  been 
recorded.  With  actual  arterial  occlusion,  as  in  old  age  and 
in  thrombo-angiitis  obliterans,  there  may  arrive  a ‘status 
anginosus  cruris’,  with  more  persistent  and  intolerable  pain 
and  pallor  and  coldness  or  gangrene  of  the  toes  or  foot. 

Tlius  we  have,  alike  in  the  pectoral  and  the  peripheral 
anginas,  benign  types  of  functional  disorder  due  presumably 
toneuro-muscular  errors  of  arterial  adaptation;  graver  types 
with  disease  and  loss  of  resilience  in  the  arterial  wall;  and 
those  gravest  types  of  all  in  which  there  is  actual  vascular 
occlusion  with  secondary'  ischaemic  consequences. 

I have  laid  some  stress  upon  the  peripheral  forms  of  angina, 
for  the  analogies  are  close,  and  I cannot  but  think  that  they 
help  to  illuminate  the  pectoral  form,  to  explain  some  of  its 
symptoms,  and  to  establish  it  as  expressive  of  vascular 
disorder  or  disease  rather  than  of  any  primary  cardiac 
affection. 


Tiic  Physiology  of  Anginal  Pain 
The  cause  of  anginal  pain  has  been  a matter  for  pliilosophic 
debate  amongst  physicians  in  many  generations.  Clinical 
observation  and  experiment  have  now  established  that 
ischaemia  of  the  heart-muscle  (as  of  the  leg-muscles  in  inter- 
mittent claudication)  is  the  essential  factor,  probably  (as 
Lewis  has  suggested)  with  accumulation  of  chemical  meta- 
bolites in  the  affected  muscle-fibres. 

Could  this  conclusion  have  been  reached  by  clinical  and 


ANGINA  PECTORIS  AND  ALLIED  SEIZURES  333 
pathological  observation  and  deduction  alone  ? If  \vc  review 
all  the  conditions  in  which  angina  pectoris  is  a symptom  and 
seek  to  isolate  a common  factor,  we  can  at  least  claim  to 
arrive  very  near  the  mark. 

In  its  worst  and  most  sustained  form  angina  pectoris 
accompanies  actual  occlusion  of  a coronary  vessel.  In  its 
next  gravest  form  it  accompanies  coronary  arteriosclerosis 
without  occlusion,  but  here  narrowing  of  the  vessel  wall  or 
inability  on  the  part  of  the  vessel  to  dilate  and  convey  an 
adequate  tide  of  blood  to  the  muscle  may  be  presumed  to 
operate.  In  * nervous  ’ and ' tobacco  ’ angina  and  in  vasovagal 
attacks  arterial  spasm  is  a reasonable  hypothesis.  In  vaso- 
vagal attacks  I have  witnessed  palpable  alterations  in  the 
radial  artery  and  remarkable  fluctuations  of  blood -pressure. 
In  aortic  incompetence,  when  due  to  syphilis,  the  mouths  of 
the  coronary  arteries  may  be  encroached  upon,  and  both  in 
the  rheumatic  and  syphilitic  types  the  intro-aortic  pressure 
ofbloodmaynotbcsuflicicntlysustainedtoflushthecoronary 
circulation  adequately  at  times  of  stress.  In  hyperthyroidism 
and  simple  paroxysmal  tachycardia,  in  both  of  which  con- 
ditions I have  noted  angina  as  an  occasional  symptom,  the 
heart  (although  we  believe  the  vessels  to  be  normal)  is  work- 
ing 4 overtime',  and  the  circulation,  as  in  the  violent  efforts 
of  health,  cannot  quite  keep  pace.  Finally,  we  arc  left  with 
the  angina  which  maj'  be  symptomatic  both  of  pernicious 
and  of  other  types  of  anaemia,  and  which  can  occur  in  cases 
lacking  nil  evidence  of  cardiac  or  arterial  disease  and  all  the 
other  factors  mentioned  above,  excepting  only  the  poverty 
of  the  blood-supply  to  the  heart  relative  to  the  demands  put 
upon  it  during  a phase  of  increased  work.  We  are  thus  left 
with  cardiac  anaemia  or  ischaemia  as  the  common  factor. 

Prognosis 

Prognosis,  always  a most  difficult  branch  of  our  art,  must 
depend  to  some  extent  upon  the  group  to  which  we  relegate 
ourcn.se.  In  the  ncrvousnndanacmic  types  of  angina  pectoris, 
in  some  of  the  mild  post-infective  types,  and,  perhaps,  in 
some  associated  with  transient  or  developing  high  blood- 
pressure,  the  outlook  as  regards  life  and  return  to  health 


331  ANGINA  PECTORIS  AND  ALLIED  SEIZURES 
may  be  quite  good.  In  the  middle-aged  type  with  arterial 
disease  it  must  always  be  guarded,  and  the  more  so  if  there 
is  any  clinical  or  electrocardiographic  evidence  of  structural 
change  in  the  heart.  In  the  absence  of  such  evidence,  and  if 
a suitable  mode  of  life  can  be  enjoined,  the  outlook  need  not 
of  necessity  be  gloomy.  In  the  third  group  with  coronary 
occlusion  the  prognosis  is  often  obviously  and  immediately 
very  bad,  or  even  if  recovery  from  the  acute  phase  follows, 
life  is  shortened.  It  is  established,  however,  that  recoveries 
and  even  a return  to  a normal  way  of  life  may  follow  the 
plugging  of  a smaller  branch  and  even  some  of  the  graver 
varieties  of  status  anginosus  which  entitle  us  to  presume 
a considerable  myocardial  infarct. 

The  prognosis  in  the  peripheral  forms  of  * angina  ’ must  also 
depend  on  the  presence  or  absence  of  organic  change  in 
the  arteries  affected,  and  is  obviously  gravest  when  arterial 
thrombosis  has  occurred. 


XXV 

A NOTE  ON 

JOHN  HUNTER’S  CARDIAC  INFARCT1 


Tire  past  ten  years  Jiavc  witnessed  a steadily  growing  out- 
put of  literature  relating  to  coronary  thrombosis  and  cardiac 
infarction.  Extensive  surveys  of  clinical  and  pathological 
material,  together  with cnrdiologicnlstudics,hnve  established 
and  defined  the  syndrome  which  characterizes  this  grave 
vascular  accident,  and  indicated  its  relationships  with  angina 
pectoris.  We  now  know  that  the  status  nnginosns  generally 
proclaims  a coronary  occlusion,  and  that,  notwithstanding 
the  gravity  of  the  event  and  its  high  immediate  mortality, 
survival  is  common,  and  a return  to  a lire  of  modified  or  even 
full  activity  not  impossible.  From  the  descriptions  of  anginal 
eases  left  to  us  by  the  great  masters,  includiug  Latham, 
Osier,  Clifford  Allbutt,  and  Mackenzie,  it  is  possible  to  select 
indubitable  earlier  examples  of  seizures  due  to  this  cause. 
It  is  noteworthy  that  Hoberden  himself  mentioned  a few 
cases  in  which  the  pain  persisted  for  hours  or  days. 

Recollecting  the  minuteness  of  the  clinical  detail  in  Sir 
Everard  Home’s  account  of  Hunter’s  illnesses,  it  occurred 
to  me  to  re-examine  the  narrative  of  these,  and  particularly 
the  descriptions  of  his  alarming  vascular  crises.  The  story'  of 
Hunter’s  angina,  of  his  foreboding  that  his  death  might  be 
precipitated  by  any  one  who  should  anger  him,  and  of  his 
actual  demise  in  such  a circumstance,  is  common  property’, 
and  1ms  found  its  place  in  the  text-books  and  been  recounted 
to  generations  of  students.  Edward  Jenner  was  alive  to  the 
significance  of  Hunter’s  symptoms  but  kept  the  information 
from  his  friend.  It  is  not,  I believe,  so  widely  recognized 
that  his  very'  first  seizure  was,  In  nil  probability',  due  to  a 
coronary'  thrombosis;  that  he  survived  it  for  20  years;  and 
that,  on  examination  after  death,  two  fibrotic  scan  were 
found  in  the  wall  of  Ins  heart. 

The  descriptions  which  follow  are  drawn  from  Joseph 
* tmtert,  IOCS.  {.  SW5. 


336  A NOTE  ON  JOHN  HUNTER’S  CARDIAC  INFARCT 
Adams’s  Memoirs  of  the  Life  and  Doctrines  of  the  late  John 
Hunter,  Esq.  (London,  1817),  in  which  the  author  includes 
full  quotations  from  Sir  Everard  Home's  Life.  Sir  Everard 
Home’s  account  was  based  on  observations  of  his  symptoms 
noted  by  Hunter  himself  at  the  time  of  their  occurrence,  or 
dictated  to  Sir  Everard  Home  when  he  was  too  ill  to  write, 
I have  italicized  some  of  the  more  apposite  passages. 

‘In  the  spring  of  17G9,  In  his  forty-first  year,  he  had  o regular  fit  of 
the  gout,  which  returned  the  three  following  springs,  hut  not  In  the 
fourth ; and  in  the  spring  of  1773,  having  met  with  something  which 
very  forcibly  affected  his  mind,  he  was  attacked,  at  ten  o’clock  in  the 
forenoon,  with  a pain  in  the  stomach,  about  the  pylorus;  it  was  the 
sensation  peculiar  to  those  parts,  and  become  so  violent,  that  he 
tried  change  of  position  to  procure  ease;  he  sat  down,  then  walked, 
laid  himself  down  on  the  carpet,  then  upon  cliairs,  but  could  find  no 
relief.  He  took  a spoonful  of  tincture  of  rhubarb  with  30  drops  of 
laudanum,  without  the  smallest  benefit.  While  he  was  walking  about 
the  room,  he  cast  his  eyes  on  the  looking-glass,*  and  observed  his 
countenance  to  be  pale,  his  Ups  white,  giving  the  appearance  of  a 
dead  man : this  alarmed  him,  and  led  him  to  feel  for  his  pulse ; but  he 
found  none  in  cither  arm.  He  now  thought  his  complaint  serious. 
Several  physicians  of  his  acquaintance  were  then  sent  for:  Dr.  William 
Hunter,  Sir  George  Raker,  Dr.  Huck  Saunders,  and  Sir  William 
Fordyce,  all  came,  but  could  find  no  pulse ; the  pain  still  continued, 
and  he  found  himself  at  times  not  breathing.  Being  afraid  of  death 
soon  taking  place  if  he  did  not  breathe,  he  produced  the  voluntary 
act  of  breathing,  by  working  his  lungs  by  the  power  of  the  will; 
the  sensitive  principle,  with  all  its  effects  on  the  machine,  not  being 
in  the  least  affected  by  the  complaint.  In  this  state  he  continued  for 
three-quarters  of  an  hour,  in  which  time  frequent  attempts  were 
made  to  feel  the  pulse,  but  in  vain;  however,  at  last,  the  pain 
lessened,  and  the  pulse  returned,  although  at  first  but  faintly,  and 
the  involuntary  breathing  began  to  take  place.  While  in  this  state, 
he  took  Madeira,  brandy,  ginger,  Ac.,  but  did  not  believe  them  of  any 
service,  as  the  return  of  health  was  very  gradual ; in  two  hours  he 
was  perfectly  recovered.’ 

Hunter  was  aged  45  at  the  time.  The  restlessness  which 
he  showed  in  the  attack  is  now  known,  in  contradistinction 
to  the  strict  immobility  of  ordinary  angina,  to  be  a not  un- 
common feature  of  coronary  thrombosis.  The  reference  of 
pain  to  the  epigastrium  is  also  a recognized  feature,  and  may 
sometimes  lead  to  a faulty  diagnosis  of  acute  abdominal 
disease.  Writing  a hundred  years  ago  Joseph  Adams  was 


A NOTE  ON  JOHN  HUNTER’S  CARDIAC  INFARCT  337 
sage  enough  to  argue*  and  in  opposition  to  Hunter’s  own 
idea,  that,  although  the  pain  was  apparently  in  the  stomach, 
the  actual  seat  of  it  was  in  the  heart. 

‘That  the  disease  was  In  the  heart  can  now  admit  of  no  doubt: 
the  cessation  of  the  pulse  is  what  might  be  expected  from  violent 
inflammation,  as  will  be  hereafter  explained ; but  the  strongest  proof 
that  the  heart  at  that  time  suffered  an  alter  at  ion  in  its  structure,  the  effect 
of  inflammation,  is,  that  for  the  remainder  of  his  life  theyatient  suffered 
all  the  effects  of  angina  pectoris. , . 

In  177G  Hunter  had  a serious  illness  in  which  vertigo  and 
sickness  played  a prominent  part.  In  1785  he  had  another 
serious  illness. 

’About  the  beginning  of  April  1785  (Sir  Evcmrd  Home  informs  us), 
he  was  attacked  w ith  a spasmodic  complaint,  which  at  first  was  slight, 
but  became  afterwards  very  violent,  and  terminated  in  a fit  of  the 
gout  In  the  ball  of  the  great  toe;  this,  like  his  other  attacks,  was 
brought  on  by  anxiety  of  mind.  The  first  symptom  was  a sensation 
of  the  muscles  of  the  nose  being  in  action ; but  whether  they  really 
were,  or  not,  lie  was  never  able  to  determine.  This  sensation  returned 
at  intervals  for  about  n fortnight,  attended  with  nn  unpleasant  sensa- 
tion in  the  left  side  of  the  face,  lower  jaw,  and  throat,  which  seemed 
to  extend  into  the  head  on  tliat  side,  and  down  the  left  arm.  as  low 
as  the  ball  of  the  thumb,  where  it  terminated  nil  at  once : these  sensa- 
tions sverc  not  constant,  but  returned  at  irregular  times ; they  became 
soon  more  violent,  attacking  the  head,  face,  and  both  sides  of  the 
lower  jaw,  giving  the  idea  that  the  face  was  swelled,  particularly  the 
checks,  and  sometimes  slightly  affected  the  right  arm.  After  they 
had  continued  for  a fortnight,  they  extended  to  the  sternum,  produc- 
ing the  same  disagreeable  sensations  there,  and  giving  the  feel  of  the 
sternum  being  drawn  backwards  towards  the  spine,  as  well  as  that 
of  oppression  in  breathing,  although  the  action  of  breathing  was 
attended  with  no  real  difilculty:  at  these  times  the  heart  seemed  to 
miss  a stroke ; and  upon  feeling  the  pulse,  the  artery*  was  very'  much 
contracted,  often  hardly  to  be  felt,  and  every  now  and  then  the  pulse 
was  entirely  itopt.  He  was  afterwards  attacked  with  a pain  in  the 
l>ack,  about  tliat  part  where  the  oesophagus  passes  through  the  dia- 
phragm, the  sensation  being  tliat  of  something  scalding  hot  passing 
down  the  oesophagus,  lie  was  next  seized  with  a pain  in  the  region 
or  the  heart  itself;  and  Last  of  all,  with  a sensation  In  the  left  side, 
nearly  in  the  scat  of  the  great  end  of  the  stomach,  attended  with 
considerable  eructations  of  wind  from  tliat  viseus:  these  seemed  to 
be  rather  spasmodic  than  n simple  discharge  of  wind,  a kind  of  mix- 
ture of  hiccough  and  eructation,  which  last  symptoms  did  not  accom- 
pany the  former,  but  came  on  by  themselves.  In  every*  attack  there 
X 


338  A NOTE  ON  JOHN  HUNTER’S  CARDIAC  INFARCT 
was  a raw  sore*  fed,  as  jf  the  fauces  were  excoriated.  Ail  these 
succeeding  symptoms  (those  in  the  stomach  and  nose  only  excepted) 
were  in  addition  to  the  first,  for  every  attack  began  with  the  first 
symptoms.  The  complaint  appeared  to  be  in  the  vascular  system,  for 
the  larger  arteries  were  sensibly  contracted,  and  sore  to  the  touch, 
os  far  as  they  could  be  touched,  principally  in  the  left  arm;  the  urine 
at  those  times  was  in  general  very  pale, 

* These  symptoms  increased  in  violence  at  every  return,  and  the  attack 
which  was  the  most  violent  came  on  one  morning  about  the  end  of  April, 
and  lasted  about  two  hours.  It  began  as  the  others  had  done , but  having 
continued  about  on  hour,  the  pain  became  excruciating  at  the  apex  of  the 
heart;  the  throat  was  so  sore  as  not  to  allow  of  an  attempt  to  swallow  any 
thing,  and  the  left  arm  could  not  bear  to  be  touched,  the  least  pressure 
upon  it  giving  pain;  the  sensation  at  the  apex  of  the  heart  was  that  of 
burning  or  scorching,  which,  by  its  violence,  quite  exhausted  him,  and  he 
sunk  into  a sicoon  or  doze,  which  lasted  about  ten  minutes,  after  which 
he  started  up,  without  the  least  recollection  of  what  had  passed,  or  of  his 
preceding  illness.  I was  with  him  during  the  whole  of  this  attack,  and 
never  saw  any  thing  equal  to  the  agonies  he  suffered;  and  when  he  fainted 
away,  I thought  him  dead,  as  the  pain  did  not  seem  to  abate,  but  to  carry 
him  off,  having  first  previously  exhausted  him. 

‘He  then  fell  asleep  for  half  an  hour,  and  awoke  with  a confusion 
in  his  bead,  and  a faint  recollection  of  something  like  a delirium ; this 
went  oH  in  a few  days. 

‘The  affections  above  described  were,  in  the  beginning,  readily 
brought  on  by  exercise;  and  he  even  conceived,  that  if  he  had  con- 
tinued at  rest,  they  would  not  have  come  on:  but  they  at  last  seized 
him  when  lying  in  bed,  and  in  his  sleep,  so  as  to  awaken  him.  Affec- 
tions of  the  mind  also  brought  them  on ; but  coolly  thinking  or  reason- 
ing did  not  appear  to  have  that  effect.  While  these  complaints  were 
upon  him,  his  face  was  pale,  and  had  a contracted  appearance, 
making  him  look  thinner  than  ordinary';  and  after  they  went  off, 
his  colour  returned,  and  his  face  recovered  its  natural  appearance.’ 

This  description  clearly  refers  to  a further  series  of  vascu- 
lar storms  of  a critical  kind.  May  they  possibly  have  accom- 
panied a second  coronary  thrombosis  ? This  illness  laid  him 
low  from  the  beginning  of  April  until  the  latter  part  of  May, 
and  ended  with  an  attack  of  gout.  After  it  he  remained 
more  than  ever  subject  to  the  angina  of  effort  or  emotion. 

In  1789  He  suffered  a lass  af  memory  and  mare  vertigo. 
Between  1791  and  1793  his  anginal  attacks  became  increas- 
ingly frequent  and  more  prolonged,  and  arrived  for  lesser 
causes. 

4 On  the  16th  of  October  1703,  when  in  Ida  usual  state  of  health, 


A NOTE  ON  JOHN  HUNTER’S  CARDIAC  INFARCT  IW9 
he  went  to  St.  George’s  Hospital , and  meeting  with  some  things  which 
irritated  his  mind,  and  not  being  perfectly  master  of  the  circum- 
stances, lie  withheld  his  sentiments;  in  which  state  of  restraint  he 
went  into  the  next  room,  and  turning  round  to  Dr.  Robinson,  one  of 
the  physicians  of  the  hospital",  he  gave  n deep  groan,  and  dropt  down 
dead  i ' 

The  body  tvas  examined  after  death,  and  the  findings  in 
regard  to  the  heart  were  reported  as  follows: 

‘Tile  pericardium  was  very  unusually  thickened,  which  did  not 
allow  it  to  collapse  upon  being  opened ; the  quantity  of  water  con- 
tained in  it  was  scarcely  more  than  is  frequently  met  with,  although 
it  might  probably  exceed  that  which  occurs  in  the  most  healthy  state 
of  these  parts.  The  heart  itself  was  very  small,  appearing  too  little 
for  the  cavity  In  which  it  lay,  and  did  not  give  the  idea  of  its  being 
the  effect  of  an  unusual  degree  of  contraction,  but  more  of  its  having 
shrunk  in  its  size.  Upon  the  under  surface  of  the  left  auricle  and  ven- 
tricle, there  were  two  spaces  nearly  an  inch  and  half  square,  which  i cere 
of  a while  colour,  with  an  opaque  appearance,  and  entirely  distinct  from 
the  general  surface  of  the  heart:  these  two  spaces  were  covered  by  an  exuda- 
tion of  coagulating  lymph,  which  at  some  former  period  had  been  the 
result  of  inflammation  there.  The  muscular  structure  of  the  heart  sms 
paler  and  looser  In  Its  texture  than  the  other  muscles  In  the  body. 
There  were  no  congula  in  any  of  its  cavities.  The  coronary  arteries 
hn<l  their  branches  which  ramify  through  the  substance  of  the  heart 
in  the  state  of  bony  tubes,  which  were  with  difficulty  divided  by  the 
knife,  and  their  transverse  sections  did  not  collapse,  but  remained 
open.  . . . The  semilunar  valves  of  the  aorta  had  lost  their  natural 
pliancy,  the  previous  stage  to  In-coming  bone,  and  in  several  spots 
there  were  evident  ossifications.  The  aorta,  immediately  Inyond  the 
semilunar  valves,  had  its  cavity  larger  than  usual,  putting  on  the 
appearance  of  an  incipient  nncurism:  this  unusual  dilatation  ex- 
tended for  some  way  along  the  ascending  aorta,  but  did  not  reach  so 
far  ns  the  common  trunk  of  the  axillary  and  carotid  artery.  The  in- 
crease of  capacity  of  the  artery  might  be  about  onc-third  of  its  natural 
area;  and  the  internal  membrane  of  this  part  had  lost  entirely  the 
natural  polish,  and  was  studded  over  with  opaque  white  spots,  raised 
higher  than  the  general  surface. . . 

To  this  account  Joseph  Adams  added  the  following 
commentary: 

* The  opnke  spot  in  the  heart  was  probably  formed  during  the  severe 
illness  of  1773,  at  which  time  the  heart  refused  to  act,  the  invariable 
consequence  or  high  inflammation  In  a muscular  part.  Such  Is  the 
immediate  effect  during  the  severe  paroxysm  of  inflammation  In  the 
heart.  The  consequences  for  the  remainder  of  life  must  depend  on 


340  A NOTE  ON  JOHN  HUNTER'S  CARDIAC  INFARCT 
the  alteration,  if  any,  which  had  taken  place  from  the  inflammation. 
Sometimes  the  heart  never  recovers,  and  the  circulation  is  carried  on 
feebly  till  the  patient  expires,  without  any  external  cause : sometimes 
the  heart  is  dilated  by  the  afilux  of  blood  on  which  it  is  at  first  unable 
to  contract,  and  after  a time  contracts  with  irregularity,  from  on 
incapacity  to  acquire  its  original  form.  In  Mr.  Hunter’s  ease,  from 
an  alteration  in  its  texture,  its  actions  became  irregular;  and  conse- 
quently the  action  of  the  lungs.  This  constitutes  angina  pectoris, 
with  which,  Sir  Everord  Home  informs  us,  Mr.  nunter  was  afllictcd 
for  the  last  20  years  of  his  life,  the  exact  period  of  this  illness.’ 

If  it  be  accepted — and  it  is  difficult  to  offer  any  alterna- 
tive explanation — that  Hunter’s  first  seizure  was  due  to  a 
cardiac  infarction,  it  is  surely  a most  remarkable  feature  of 
his  case  that  he  should  not  only  have  survived  it  for  20  years, 
but  that  for  the  greater  part  of  that  time  he  should  have 
been  able  to  devote  himself  to  labours  which  continued  to 
add  lustre  to  his  earlier  fame.  This  chapter  of  Hunter’s  life 
which  is  concerned  with  his  illnesses  affords  us  a glimpse  of 
the  great  strength  of  will  and  the  scientific  interest  with 
which  he  constantly  met  them,  and  only  serves  to  increase 
our  admiration  of  the  man.  I do  not  know  whether  any 
parallel  case  can  be  quoted,  but  for  the  benefit  of  the  physi- 
cian faced  with  the  delicate  task  of  prognosis  in  this  grave 
and  disturbing  malady  it  is  at  least  gratifying  to  record  that 
it  may  sometimes  be  consistent  -with  long  years  of  useful 
activity. 


XXVI 

THREE  CASES  OF  CARDIAC  DISTRESS1 

The  heart,  embarrassed  by  disease,  complains  in  various 
ways.  The  symptoms  by  which  we  recognize  its  complaint 
may  be  referred  to  the  organ  itself,  ns  in  the  case  of  pain  or 
palpitation,  or  to  other  organs  and  tissues  whose  circulation 
is  impaired  in  consequence  of  the  cardiac  disability.  Thus, 
you  are  all  famitiar  with  dyspnoea,  oedema,  cyanosis,  and 
engorgement  of  the  liver  as  manifestations  of  heart  failure. 

The  three  cases  from  ClinicalWard  which  I bring  before  you 
to-day  arc  undoubted  examples  of  cardiac  or  cardiovascular 
disease  with  distress  or  failure,  but  the  pictures  presented 
by  them  are  so  different  that  you  would  at  once  surmise, 
and  rightly,  that  each  must  express  a different  pathology. 
Each  case  holds  for  us  lessons  in  respect  ordingnosis,  prognosis, 
and  treatment  which  I shall  endeavour  to  unfold  to  you  in 
considering  their  several  histories. 

The  first  is  that  of  n married  woman  aged  13,  who  was 
admitted  to  Miriam  Ward  in  April  1928.  She  had  rheumatic 
fever  at  the  age  of  21,  and  has  nine  children  olive  and  well; 
two  others  died  in  infancy.  In  the  autumn  of  1927  we  obtain 
the  first  clear  account  of  cardiac  distress,  for  she  was  admitted 
to  the  Rotlicrhithc  Infirmary  for  dyspnoea  arid  pain  in  the 
left  chest,  and  remained  there  for  a month.  Since  then  she 
has  rested  at  home,  but,  becoming  less  well  latterly  with 
cough,  pain  round  the  waist,  dyspnoea  on  effort,  and, 
finally,  a sharp  pain  on  breathing  in  tire  left  chest,  she  was 
sent  up  to  Guy's.  Her  pulse  on  admission  was  found  to  be 
rapid  and  irregular,  the  excursions  at  the  wrist  were  of  vary- 
ing size  and  some  pulsations  failed  to  reach  the  wrist.  IVe 
were  of  the  opinion  that  she  lmd  auricular  fibrillation,  but 
at  the  same  time  noted  frequent  short  paroxysmal  phases 
in  which  the  rhythm  appeared  to  be  regular.  This  was  of 
interest,  as  Dr.  Campbell's  first  elect rorardiogrnm  showed 

* f/uy'i  llotp.  Vaxrtte,  JP23.  *115.  302. 


3 12  THREE  CASES  OP  CARDIAC  DISTRESS 
the  presence  of  auricular  flutter,  although  under  treatment 
with  digitalis  this  was  quickly  replaced  by  fibrillation.  Fibril- 
lation as  a late  consequence  of  rheumatic  fever  is  almost 
always  an  association  of  mitral  stenosis,  and  we  thought  we 
had  good  support  for  a diagnosis  of  mitral  stenosis  in  the 
remarkably  deep  red  colour  of  her  lips,  which  you  can  see  for 
yourselves  to-day,  and  which  the  patient  assures  us  is  not 
due  to  the  use  of  a lipstick.  The  heart  was  enlarged  and 
there  was  a systolic  murmur  at  the  apex,  but  at  first  we  could 
determine  no  confirmatory  pre-systolic  thrill  or  rumbling 
murmur.  Other  findings  included  considerable  enlargement 
of  the  liver,  albuminuria,  and  a dry  localized  pleuritic  friction 
at  the  left  base  to  account  for  her  pain.  This,  we  thought, 
might  be  due  to  a small  pulmonary  infarction,  and  held  as 
further  evidence  in  favour  of  mitral  stenosis.  Improvement 
rapidly  followed  rest  in  bed  and  digitalization.  The  liver 
margin  has  retired,  the  albumin  has  disappeared,  the  urinary 
output  has  increased,  the  pulse-rate  has  fallen,  and  j'ou  can 
now  feel  and  hear  for  yourselves  a thrill  and  a diastolic 
murmur.  Her  full  diagnosis  might  therefore  be  stated  briefly 
as  follows:  ‘Rheumatic  carditis.  Mitral  stenosis.  Auricular 
flutter,  givingplacetofibrillation.  Hepaticand  renal  engorge- 
ment. Pulmonary  infarction.  ’ I should  like  to  impress  upon 
you  that  a large  part  of  this  information  could  be  gleaned 
from  a glance  at  her  lips  and  a finger  on  her  pulse  after 
listening  to  the  account  of  her  symptoms,  and  that  first 
impressions,  often  valuable  but  never  wholly  to  be  trusted, 
were  in  this  case  fully  borne  out  by  the  subsequent  findings. 
How  is  it  that  she  was  able  to  support  eleven  pregnancies 
without  mishap?  We  are  commonly  taught  that  mitral 
stenosis  must  in  many  cases  be  regarded  as  a contra-indica- 
tion to  future  pregnancies  because  of  the  added  strain  and 
risk  which  these  entail.  I think  it  is  reasonable  to  conclude 
from  the  history  of  this  case  that,  although  mitral  stenosis 
has  been  present  for  years,  the  faulty  rhythm  and  muscle 
failure  are  of  much  more  recent  origin. 

The  case  exemplifies  well  the  rapid  improvement  which 
may  take  place  with  rest  and  digitalis.  It  is  now  important 
that  she  should  curtail  her  domestic  activities,  and  witli  a 


THREE  CASKS  OF  CARDIAC  DISTRESS  3 W 
growing  family  this  can  fortunately  be  arranged.  It  is  also 
important  that  she  should  continue  to  take  a small  dose  of 
digitalis  indefinitely.  So  often  I find  that  the  drug  has  been 
discontinued  when  a certain  point  of  improvement  has  been 
reached.  I know  no  contra-indication  in  tolerant  patients 
to  the  taking  of  small  doses  over  very  long  periods,  and  15 
to  20  minims  of  the  tincture  daily  may  well  help  to  protect 
this  patient  against  recurrences  of  her  recent  illness. 

This  type  of  case  will  he  familiar  to  you  all.  The  other 
two  are  more  dramatic  and  less  common,  but  you  should  be 
acquainted  with  the  clinical  pictures  which  they  present. 

Mr.  H N , aged  55,  a porter,  was  admitted  to 

John  Ward  for  collapse  and  extreme  dyspnoea.  At  the  age 
of  0 he  had  extensive  syphilitic  ulceration  of  the  right  arm, 
of  which  he  bears  the  scars.  We  have  no  knowledge  of  how 
the  disease  was  acquired.  Two  and  a half  years  ago  he  was 
taken  to  hospital  for  an  attack  similar  to  that  for  which  he 
was  recently  admitted.  Before  that  he  had  had  slighter 
attacks,  but  it  is  noteworthy  that  he  has  since  remained  at 
work  until  the  very  day  of  his  admission.  He  was  admitted 
in  the  early  hours  of  the  morning  of  27  April,  having  been 
found  in  a collapsed  condition  in  the  street.  His  colour  was 
a greyish-blue;  his  skin  was  cold  and  covered  with  sweat; 
he  had  no  pain,  but  breathing  was  laboured  and  ‘accom- 
panied by  a continuous  bubbling  sound  ’ ; froth  was  trickling 
from  the  comer  of  his  mouth ; the  pulse  was  irregular,  and 
its  rate  140  to  the  minute;  respirations  30  to  the  minute; 
the  apex  beat  was  in  the  fifth  space,  1 1 inches  outside  the 
nipple  line;  pmccordinl  dullness  extended  to  the  right  of 
the  sternum.  The  liver  margin  was  tender.  He  was  given 
nasal  oxygen,  and  one-hundredth  of  a grain  each,  hypo- 
dermically, of  atropine  and  strophanthin,  and  8 ounces  of 
blood  were  withdrawn  from  his  median  basilic  vein.  From 
looking  and  feeling  desperately  ill,  his  appearance  and 
sensations  steadily  improved,  so  that  when  I first  saw  him 
about  12  hours  later  he  was  quite  comfortable  and  the 
bubbling  In  bis  lungs  had  all  sulfided.  As  you  sec,  he  is  now 
free  from  all  embarrassment,  but  by  bis  Own  pan's  pulse  and 
aortic  murmurs  you  can  recognize  a part  of  the  underlying 


344  THREE  CASES  OF  CARDIAC  DISTRESS 
trouble.  The  history  is  that  of  the  condition  known  as  acute 
pulmonary  oedema.  Pulmonary’  oedema  akin  to  this  may’ 
result  from  inhalation  of  irritant  gases  such  ns  phosgene  gas, 
firstusedasa  lethal  weapon  in  the  1914-18  war,  and  may  very 
rarely  be  symptomatic  of  an  acute  pulmonary  infection.  But 
the  cases  encountered  in  practice  are  usually  a consequence 
of  cardio-artcrial  disease,  and  the  oedema  is  thought  to  be  a 
result  of  serous  transudation  from  the  smaller  pulmonary’ 
vessels  in  conditions  in  which  the  left  ventricle  finds  itself 
unable  to  transmit  the  whole  output  of  the  right  ventricle — 
in  fact  of  acute  left  ventricular  failure.  In  support  of  this 
hypothesis  we  see  acute  pulmonary  oedema,  principally  in 
cases  of  arterial  and  renal  disease  with  high  blood-pressure 
and  in  aortic  incompetence,  conditions  in  which  the  left 
ventricle  is  overtaxed.  This  man  has  a to-and-fro  murmur 
in  the  aortic  area  which  we  believe  to  be  due  to  syphilitic 
aortitis — his  Wassermann  reaction  is  strongly  positive,  and 
you  will  remember  his  early  history ; in  addition,  his  blood- 
pressure  has  been  recorded  as  high  as  185  systolic,  100  dia- 
stolic. Thecharactcristicfeaturesofacutcpulmonary  oedema 
are  sudden  onset,  rapid  development  of  dyspnoea  and  distress 
with  moist  sounds  all  over  the  chest,  and  the  outpouring, 
sometimes  in  enormous  quantities,  of  a white  or  slightly 
blood-stained  frothy  fluid,  resembling  the  spume  on  the  lips 
of  an  over-driven  horse.  The  treatment  in  grave  eases  should 
include  continuous  intranasal  oxygen,  a hypodermic  injection 
of  morphine  with  atropine,  and  venesection.  From  lesser 
attacks  the  patient  may  recover  spontaneously ; from  seem- 
ingly hopeless  attacks,  in  which  drowning  seems  imminent, 
he  may  be  dramatically  reclaimed  by  timely  aid  to  survive 
for  longer  or  shorter  periods.  As  the  underlying  cause  is 
generally  some  serious  organic  change  in  the  heart  and 
arteries,  the  ultimate  prognosis  can  seldom  be  good. 

Our  third  case  is  that  of  a man  aged  54.  He  has  consumed 
too  much  alcohol  in  the  past,  and  was  once  in  Guy’s  for  a 
fractured  leg ; otherwise  his  medical  history  was  uneventful 
until  six  montlis  ago.  He  then  began  to  notice  a sense  of 
retrosternal  discomfort  on  mounting  stairs  or  with  other 
exertion.  At  times  there  was  actual  pain,  but  this  always 


THREE  CASES  OF  CARDIAC  DISTRESS  345 
disappeared  immediately  with  rest.  On  the  morning  or  19 
April  he  was  suddenly  seized  at  his  place  of  business  with  a 
violent  retrosternal  pain.  lie  had  to  He  down,  but  could  not 
remain  still,  and  rolled  about  in  the  extremity  of  Ins  agony, 
lie  was  brought  to  the  surgery  in  a state  of  collapse  with  a 
rapid,  feeble  pulse.  Amyl  nitrite  gave  instant  but  incomplete 
relief.  lie  went  home,  but  had  a return  of  pain  nnd  was 
admitted  the  next  day.  lie  was  noted  as  nervous,  shaky, 
and  plethoric.  Ilis  pain  was  still  located  behind  the  middle 
of  the  sternum.  His  pulse  was  98  to  the  minute  and  regular. 
His  blood-pressure,  which  had  been  1 CO  systolic  in  the  surgery 
on  the  previous  day,  had  fallen  to  NO.  The  next  day  it  was 
120  and  the  next  day  90 — a very  low  figure  for  a man  of  Ins 
build — at  which  it  has  since  remnined.  The  impulse  was 
neither  visible  nor  palpable;  the  left  border  by  percussion 
was  4 inches  from  the  midlinc.  The  most  striking  physical 
sign,  and  this  has  persisted,  as  you  shall  hear  for  yourselves, 
was  the  inaudibility  of  the  heart-sounds.  With  very  careful 
attention  they  can  now  just  be  heard,  faint  nnd  far  away  nnd 
equalized.  There  is  no  considcrablecmphyscma  or  other  inter- 
vening cause  to  explain  this,  nnd  we  believe  it  to  be  due  to  a 
serious  myocardial  damage.  For  many  days  after  admission 
the  chart  shows  pyrexia,  gradually  settling  by  lysis.  There 
was  a Icucocytosis  at  first  of  29,000  cells  per  c.mm.,  which, 
in  concert  with  the  declining  temperature,  has  gradually 
fallen  to  11,500.  The  history  of  onset  nnd  the  symptoms  nnd 
signs  which  I have  dcscrilxxl  arc  characteristic  of  coronary 
thrombosis  with  cnrdiac  infarction.  Of  this  condition  there 
arc  at  least  twelve  important  manifestations,  including: 

(1)  Onset  with  status  anginosus,  or  rapidly  repented 
anginal  seizures  at  rest,  although  it  is  believed  that 
coronary  occlusion  without  pain  can  also  occur. 

(2)  Restlessness  in  the  nttnek,  instead  of  the  usual  im- 
mobility of  angina  pectoris. 

(3)  Failure  or  amyl  nitrite,  anti  relief  with  difficulty  even 
by  morphine,  large  or  frequent  doses  often  living 
necessary. 

(4)  Shock -like  symptoms  in  the  graver  eases. 


348  THREE  CASES  OF  CARDIAC  DISTRESS 

(5)  Epigastric  instead  of  sternal  pain,  with  simulation  of 
an  acute  abdominal  catastrophe  in  some  coses. 

(6)  Fever  following  the  attack,  transient  or  lasting  for 
several  days. 

(7)  Pericardial  friction,  usually  very  transient. 

(8)  A falling  blood-pressure. 

(9)  Development  of  signs  and  symptoms  of  congestive 
failure  in  the  graver  cases. 

(10)  Faintness  and  equalization  of  the  heart-sounds  and 
sometimes  arrhythmia. 

(11)  Lcucocytosis. 

(12)  Certain  electrocardiographic  changes  indicative  of 
myocardial  damage. 

Of  these  twelve  manifestations,  no  less  than  eight,  includ- 
ing the  electrocardiographic  changes — which  Dr.  Maurice 
Campbell  reports  as  typical — were  recorded  in  the  case  of 
this  man.  What  are  we  to  presume  is  the  associated  morbid 
change?  We  can  with  some  confidence  assert,  with  our 
growing  knowledge  of  the  syndrome,  that  he  has  a branch 
of  a coronary  artery  occluded  by  a thrombus,  the  thrombus 
being  secondary  to  coronary  atheroma,  and  that  he  has 
ischaemia  with  necrosis  of  a part  of  his  ventricular  wall. 
Although  he  is  now  comfortable,  the  prognosis  in  this  case 
is  not  good,  and  clearly  when  a large  branch  is  blocked  the 
ultimate  outlook  is  always  bad.  But  I believe  it  to  be  wrong 
to  take  a gloomy  view  in  ever)’  case  of  coronary  thrombosis. 

I have  notes  of  patients  who  led  active  lives  for  upwards 
of  ten  years.  John  Hunter  lived  and  worked  for  twenty 
years  after  his.  In  the  initial  stage  treatment  must  include 
absolute  rest  in  bed  for  an  adequate  period,  the  duration 
being  never  less  than  several  weeks  and  regulated  by  the 
severity  of  the  initial  symptoms,  the  progress  of  the  case, 
and  other  evidences.  For  the  pain  morphine  should  be  given. 
Small  doses  of  digitalis  are  thought  to  be  desirable  if  there 
is  tachycardia  or  arrhythmia. 

I have  shown  you  our  three  cases  of  cardiac  distress.  The 
first  was  admitted  for  pleuritic  pain  and  dyspnoea  on  effort; 
the  second  for  sudden  and  urgent  dyspnoea  and  obvious 


THREE  CASES  OF  CARDIAC  DISTRESS  317 
oedema  of  the  lungs;  the  third  for  intense  and  sustained 
retrosternal  pain,  followed  by  pyrexia,  a falling  blood-pres- 
sure, and  an  inaudibility  of  the  heart-sounds  so  striking  that 
I have  brought  him  here  principally  for  you  to  observe  this 
sign  for  yourselves.  With  some  confidence  we  have  been  able 
to  attach  n causal  pathology  in  each  instance.  Incidental^', 
too,  these  cases  have  served  to  illustrate  some  of  the  effects 
of  the  three  commonest  causes  of  organic  cardiac  disease, 
namely,  rheumatic  fever,  syphilis,  and  arteriosclerosis. 


XXVII 

THROMBOPHLEBITIS  MIGRANS1 

Tite  occurrence  of  cases  of  phlebitis  with  thrombosis,  some- 
times widespread  and  recurrent  but  lacking  any  clear  aetio- 
logical  associations,  has  long  been  recognized.  Such  cases, 
although  not  common,  are  by  no  means  excessively  rare.  They 
are  distinct  both  in  their  history  and  in  their  course  from  those 
forms  of  thrombophlebitis  « hich  complicate  the  specfiic  fevers 
or  follow  operations  and  the  puerperium,  or  which  have 
been  recorded  in  connexion  with  syphilis,  tuberculosis,  malig- 
nant disease,  and  anaemia.  They  arc  not  due  to  varicosity 
or  other  chronic  disease  of  the  veins.  It  is  possible  that 
some  of  the  cases  of  phlebitis  formerly  ascribed  to  gout  may 
have  belonged  to  this  special  group.  Sir  James  Paget  [l] 
reported  cases  of  diffuse  superficial  phlebitis,  both  gouty  and 
non-gouty,  as  long  ago  as  18CG.  More  recently  an  interesting 
account  of  4 cases  has  been  given  by  Moorhead  and  Abraham  - 
son  [2],  under  the  title  of  ‘Thrombo-phlebitis  Migrans’,  in 
three  of  which  wandering  superficial  thromboses  of  this  kind 
were  accompanied  by  visceral  thromboses.  Five2  similar 
cases,  4 of  them  with  visceral  thromboses,  have  come  my 
way,  and  I am  sure  it  will  be  in  the  experience  of  others  to 
have  encountered  examples  of  this  condition  from  time  to 
time  in  the  ordinary'  course  of  practice.  Campbell  and  Morgan 
[8]  have  lately  recorded  a case  of  brachial  thrombophlebitis 
complicated  by  severe  headache  and  tubular  vision,  due 
possibly  to  thrombosis  of  posterior  cerebral  vessels,  and  also 
by  cardiac  symptoms  with  cardiographic  findings  suggesting 
a coronary  thrombosis.  Carey  Coombs  [4]  has  mentioned 
cases  of  coronary  thrombosis  in  association  with  peripheral 

1 Based  on  a communication  given  before  the  Association  of  Physicians 
in  London  on  C June  1030  (Lancet,  1930,  il.  731). 

* My  experience  has  since  been  increased  by  13  additional  coses,  and  I 
hare  now  seen  migratory  phlebitis  antecedent  once  to  the  discovery  ot 
deep-seated  malignancy  and  once  to  bacterial  endocarditis;  I have  also 
seen  it  In  a gouty  subject. 


THROMBOPHLEBITIS  MIGRANS  3*9 

phlebitis,  including  one  ease  in  which  n pulmonary  nnd  then 
a cardiac  thrombosis  preceded  thrombophlebitis  in  the 
thigh.  Briggs  [5]  and  Herrick  [0]  have  reviewed  the  subject 
of  wandering  phlebitis,  but  they  gave  no  account  of  visceral 
lesions. 

The  name  thrombophlebitis  migrnns  seems  to  me  admir- 
ably suited  to  the  condition.  The  process  is  essentially 
migratory,  the  lesions  showing  dissemination  both  in  space 
and  time,  as  will  be  seen  from  an  examination  of  the  ease 
reports  given  hereunder.  The  same  nomenclature  has  been 
applied  to  a rarer  condition  in  which  the  phlebitis  spreads 
gradually  along  the  course  of  a particular  vein  or  veins.  As, 
however,  this  may  he  described  more  correctly  ns  a ‘creep- 
ing’than  a‘ wandering’ process, it  would  seem  that  thrombo- 
phlebitis migrans  is  more  appropriate  to  the  disease  under 
discussion. 

Moorhead  and  Abrahnmson  expressed  themselves  ns 
unable  to  throw  any  light  on  the  aetiology  of  the  condition. 
In  one  of  their  eases,  it  is  true,  the  first  superficial  phlebitis 
followed  n mosquito  bite  on  the  same  limb  after  an  interval 
of  a week;  a month  previously,  however,  the  patient  bad 
lmd  an  unexplained  pleurisy  which,  in  the  light  of  later 
events,  may  well  have  been  due  to  a primary  pulmonary 
thrombophlebitis.  In  another  ease  the  first  phlebitis  oc- 
curred in  the  leg  three  months  after  a superficial  bum  on 
the  corresponding  foot.  In  a third  there  was  severe  pyor- 
rhoea. Owen  [7,  8]  has  sought  to  associate  the  condition 
with  influenzal  epidemics,  but  in  none  of  my  eases  nor  in 
those  described  bv  Moorhead  nnd  Abrahnmson  was  there 
any  good  reason  to  suspect  influenza  ns  on  nctiologicnl 
factor.  I am,  however,  inclined  to  agree  with  him  when  be 
suggests  that  many  of  the  obscure  pleurisies  of  practice 
associated  with  red  haemoptysis  arc  due  to  small  pulmonary 
thromboses  of  infective  origin.  The  association  in  one  of  my 
cases  with  a subsequent  bacteria!  endocarditis  (Strep. 
viridtiTu)  nnd  the  not  infrequent  association  (described 
hereunder)  with  dental  sepsis  lend  me  to  suggest  that— 
where  gout  enn  be  excluded— n phlebitis  start  ingin  oneofthe 
valves  of  n vein  nnd  consequent  upon  n transitory  bacteri- 


350  THROMBOPHLEBITIS  MIGRANS 

aemia  with  Strep,  viridans  may  prove  to  be  the  usual 

pathology  of  this  condition. 

The  cases  which  I propose  to  describe  confirm  and 
amplify  the  observations  of  Moorhead  and  Abrahamson, 
and  also  serve  to  indicate  some  of  the  difficulties  in  diagno- 
sis which  may  arise  over  the  visceral  lesions.  One  case  is 
included  in  which  there  were  symptoms  of  visceral  throm- 
boses without  the  involvement  of  any  superficial  vein. 
In  3 of  the  5 cases  there  was  good  reason  to  suspect  the 
influence  of  chronic  focal  sepsis.  The  period  within  which 
symptoms  of  wandering  thrombophlebitis  continued  to 
arrive  is  indicated  in  brackets  at  the  heading  of  each  case. 

Reports  of  Five  Cases 

Case  1.  Thrombophlebitis  affecting  both  legs  (1021-7). — A young 
man,  aged  23,  previously  in  robust  health,  first  developed  pldebitis 
in  the  calf  of  the  right  leg  in  1024.  This  was  slow  to  mend,  and  he 
eventually  had  the  vein  excised.  lie  was  then  well  until  the  first 
week  of  October  1027,  when  he  again  developed  phlebitis  in  both 
legs.  A fortnight  later  he  was  found  to  have  a tender  molar  tooth. 
This  was  extracted.  When  I first  saw  him  in  consultation  with  Dr. 
C.  Sherris  on  27  November  1927,  the  legs  had  cleared  completely,  hut 
he  had  just  developed  a fresh  phlebitis  involving  a short  segment  of 
one  of  the  veins  on  the  dorsum  of  his  right  foot.  At  one  time  he  had 
had  an  enlarged  epitrochlear  gland,  but  there  was  no  history  of 
syphilis,  and  the  Wasscrmann  reaction  was  negative.  There  was  no 
gouty  history.  A differential  blood  count  showed  no  abnormality. 
Clotting  time  was  normal.  Mr.  Kelsey  Fry,  on  clinical  and  radio- 
graphic  evidence,  advised  the  extraction  of  four  dead  teeth,  and 
reported  os  follows:  ‘Three  of  the  dead  teeth  that  I have  extracted 
showed  marked  apical  absorption,  and  as  they  had  never  been  filled, 

I must  presume  the  infection  was  blood-borne.  Were  they  the  cause 
of  the  thrombosis,  or  ore  they  due  to  the  same  cause?’  Two  years 
and  a half  have  now  elapsed  without  any  further  symptoms  of 
phlebitis  or  other  ill  health. 

Case  2.  Thrombophlebitis  affecting  one  leg,  both  lungs,  and  infra- 
abdominal  reins  (Marcb-July  1024). — A man,  aged  58,  was  submitted 
to  my  care  by  Dr.  T.  D.  H.  Holmes  for  phlebitis  of  the  right  leg, 
which  had  already  necessitated  his  lying  up  for  a month. 

For  some  months  previously  he  had  felt  ‘out  of  sorts’  and  dis- 
inclined for  work,  hut  he  had  had  no  other  illness  of  importance.  For 
ten  days  prior  to  my  first  seeing  him  he  had  had  an  almost  continuous 
stomach-ache,  but  in  the  last  two  days  both  this  and  the  leg  dis- 


352  THROMBOPHLEBITIS  MIGRANS 

ficial,  nnd  there  was  no  evidence  of  extension  to  larger  or  deeper 
vessels.  The  temperature  did  not  exceed  100°  F.  I diagnosed  pul- 
monary thrombophlebitis. 

On  the  next  day  lie  started  to  have  some  small  haemoptyses  and 
simultaneously  developed  a fresh  phlebitis  on  the  dorsum  of  his  right 
foot.  Excepting  for  transient  pains  in  the  left  axilla  and  the  left 
loin  he  had  no  further  symptoms  suggestive  of  visceral  involvement, 
but  progress  to  complete  recovery  was  interrupted  by  five  other  very 
small  thromboses  affecting  superficial  veins  of  the  left  leg  and  foot. 
During  the  earlier  phase  of  the  illness  a blood  culture  was  negative; 
the  leucocyte  count  was  12,200  cells  per  c.mm.,  whereas  he  had 
always  previously  shown  a marked  lcucopcnia ; a Streptococcus  viri- 
dans  was  grown  from  the  sputum.  Radiograms  later  showed  marked 
opacity  of  the  right  antrum,  a doubtful  right  frontal  sinus,  nnd  three 
definitely  infected  teeth.  The  infected  teeth  were  extracted.  The 
last  thrombosis  followed  a few  weeks  after  the  extractions. 

It  seemed  reasonable  to  suppose  tlrnt  this  wandering  thrombo- 
phlebitis was  a late  sequel  of  his  septic  illness  of  the  previous  year, 
and  due  to  lingering  focal  infection.  There  was  no  reason  to  consider 
gout  as  n factor. 

Case  4.  Thrombophlebitis  affecting  both  legs,  loth  lungs,  and  a cere- 
bral icin  (1024-0). — On  13  April  1029  I was  asked  to  see,  in  consulta- 
tion with  Dr.  G.  T.  Cregan,  a spinster,  aged  53,  w ho  gave  the  following 
history. 

In  1897  she  had  rheumatic  pericarditis.  In  1007  she  had  herpes  of 
the  scalp  and  developed  anginal  attacks,  for  wliich  she  saw  Sir  James 
Mackenzie.  During  the  war  period,  in  which  she  was  employed  with 
arduous  and  responsible  duties,  she  became  unfit  for  a time,  and  a 
streptococcus  was  grown  from  the  urine  In  1015  and  again  in  1017. 
In  1010  she  had  a return  of  anginal  pain  and  severe  streptococcal 
infections  of  the  throat.  Between  1010  and  1024  she  was  treated  with 
vaccines.  In  1024  she  had  an  acute  illness  with  anginal  symptoms, 
rigor,  a pulse-rate  of  140,  thrombosis  In  the  left  leg,  and  bilateral  pul- 
monary ‘embolisms’  with  haemoptysis.  In  January  1025  she  had 
otitis  media.  In  May  1028  she  had  a septic  throat  and  right-sided 
‘pleurisy’,  and  coughed  up  a little  blood.  In  September  1028  she  felt 
stiff  in  her  left  face,  her  left  hand  became  ‘woolly’,  and  she  was  sick. 
She  was  at  this  time  in  bed  for  a month  with  slight  fever.  By  Novem- 
ber 1028  she  was  again  very  ill  with  haemoptysis,  and  some  sterile 
fluid  was  aspirated  from  the  right  chest.  Her  sputum  grew  Fried- 
llinder's  bacillus,  streptococci,  and  pneumococci.  In  December  1028 
she  had  a new  thrombosis  in  the  left  leg  with  oedema.  In  January 
1020  the  right  leg  became  affected,  with  red  patches  and  a tender 
point  in  the  groin. 

The  patient  was  of  obese  habit,  and  at  the  time  of  my  examination 
both  legs  remained  slightly  swollen.  Her  tonsils  were  very  unhealthy. 


TimoMiJorjiMmiTJS  jmghaxs  353 

Grip  and  power  of  discrimination  were  poorer  In  tire  left  than  the 
right  Itand.  There  was  a family  history  of  erysipelas  affecting  her 
mother,  one  uncle,  one  aunt,  and  a brother.  1 saw  her  once  again 
subsequently,  when  she  lmd  tail  another  attack  of  tonsillitis  with 
quinsy,  hut  no  further  phlebitis. 

Cask  5.  Thrombophlebitis  affecting  abdominal  and  pulmonary  veins 
(April -July  1020). — A burly,  broad-chested  coal  magnate,  oped  49, 
after  fishing  in  Scotland,  Irecamc  shivery  and  unwcli,  hut  decider!  to 
travel  by  road  to  his  home  in  the  south  of  Kngland.  'flic  next  day  Ire 
had  epigastric  pain. 

lie  nrrived  home  on  28  April  1029  with  n temperature  of  102*  and 
pain  in  the  upjwr  abdomen  aggravated  by  coughing  and  deep  breath- 
ing. Tire  abdomen  was  then  soft  and  flaccid.  Jlv  1 May,  however,  it 
became  tense  and  distended,  and  there  were  some  rose-coloured 
spots.  At  this  time  attention  was  focuses!  on  his  nMomfiin!  condition, 
and  a few  days  later  his  doctor,  Dr.  I*.  Leslie,  called  in  Mr.  J.  L.  Joyce 
for  a surgical  opinion.  The  |K>sslbilitics  discussed  included  typhoid 
fever,  cholecystitis,  pancreatitis,  and  an  inflamed  rrtrococcal  appen- 
dix. The  pulse-rate  did  not  exceed  TO.  There  sms  no  diarrhoea  and 
no  splenic  enlargement,  Hlood  cultures  remained  sterile  and  Widal’s 
test  wu9  negative.  Total  and  differential  leneocyte  counts  showed 
no  abnormality.  Ily  5 May  the  tcmj>crature  was  falling. 

On  the  evening  of  0 May  he  sms  seized  with  very’  severe  pain  be- 
tween his  left  costal  margin  and  the  left  scapula.  At  frequent  inter- 
vals during  the  next  21  hours  he  had  agonizing  constricting  pains  In 
the  epigastrium,  so  that  breathing  sms  shallow  ami  difficult  and  he 
dared  not  move.  Simultaneously  the  temperature  rose  to  103*  and 
the  pulse  to  100.  A slight  oceipitnl  headache  transferred  itself  to  the 
frontnl  region.  I-cucoeytc  count  18,000  ceils  per  c.mtn.  I aaw  Mm  at 
10.30  p.m.  on  7 Slay  with  Dr.  l^slie  nod  Mr.  Joyce.  Now  nnd  then  he 
had  bad  spasms  of  epigastric  pain  which  caught  his  breath.  There 
were  no  signs  of  cardiovascular  disease.  There  sms  general  distension 
of  the  abdomen,  hut  no  spots  remained.  Lxceptlng  for  showing 
crowding  of  the  left  lower  ribs  with  slight  impairment  of  movement, 
the  physical  examination  was  otherwise  wholly  negative. 

I was  asked  to  see  this  patient  again  on  3 June,  at  the  end  of  the 
sixth  week  of  his  illness.  After  my  previous  visit  the  tcnqKrulurc 
lmd  at  first  gradually  settled,  but  then  tusc  again  with  a return  of 
pain  and  the  development  of  on  effusion  at  the  left  base,  l'or  a few 
•fa yt  bright  Mood  was  expectorated,  On  SO  May  the  frmperafnrr  bad 
fallen  to  normal.  Two  days  later  It  rose  again,  and  on  2 June  there 
wa*  a slight  rigor  together  with  a new  agonizing  pain  below  the  right 
nipple;  it  is  noteworthy  tliat  during  the  previous  week  the  jwtient 
lmd  experienced  a pain  at  this  paint  on  coughing  or  sneezing.  The 
condition  of  the  abdomen  had  Improved  In  the  meantime.  There  was 
no  enlargement  of  fiver  or  splttn.  ninod  culture  negative.  Sputum 

a a 


354  THROMBOPHLEBITIS  MIGRAN’S 

examination  negative.  The  fluid  previously  withdrawn  from  the  left 
chest  was  slightly  turbid  and  blood-stained,  showing  red  cells  and 
leucocytes  in  the  deposit,  but  was  sterile  on  cultivation.  A fresh 
effusion  on  the  right  side  now  gave  exactly  similar  fluid. 

I diagnosed  wandering  pulmonary  thromboses.  The  violent  spas- 
modic pains  were  exactly  like  those  described  in  Case  3.  The  fluid 
was  characteristic  of  pulmonary  infarction  and  like  that  obtained  in 
Case  2.  The  red  haemoptysis  was  typical  of  infarction.  At  no  time 
was  there  anything  suggestive  of  an  ordinary  pneumonia.  I am  in- 
clined to  the  view  tliat  the  earlier  abdominal  symptoms  were  also  due 
to  visceral  thromboses.  Although  in  the  foregoing  notes  stress  has 
been  chiefly  laid  upon  the  pulmonary  manifestations,  it  should  be 
mentioned  that  the  advisability  of  laparotomy  was  discussed  on  more 
than  one  occasion,  and  there  were  several  other  consultations,  at 
which  I was  not  present,  with  regard  to  the  proper  interpretation  of 
the  nbdominal  symptoms.  The  patient  mnde  a complete  recovery. 

Discussion 

In  the  group  formed  by  these  5 cases,  together  with  6 
others  recently  described  in  some  detail  in  the  English 
literature  (Moorhead  and  Abrahnmson  4,  Campbell  and 
Morgan  1,  Carey  Coombs  I),  there  were  8 examples  of  pul- 
monary thrombosis ; 4 clear  or  presumed  examples  of  ab- 
dominal thrombosis ; 3 probable  examples  of  cardiac  and  2 
of  cerebral  thrombosis.  Although  two  of  my  patients  had 
had  anginal  symptoms  I was  not  satisfied  that  these  were 
attributable  to  coronary  thrombosis.  In  addition  to  in- 
volvement of  both  upper  and  lower  limbs,  Moorhead  and 
Abrahamson  also  reported  cases  with  thrombophlebitis 
affecting  the  face  and  the  abdominal  wall. 

In  those  cases  in  which  pulmonary  symptoms  have  fol- 
lowed phlebitis  in  a limb  it  might  be  reasonably  suggested 
that  the  symptoms  were  due  to  small  embolisms  and  not 
to  thromboses.  Against  this  view  are  (1)  the  sequence  ‘left 
leg,  left  lung,  right  foot’  in  Case  3;  (2)  the  late  arrival 
of  the  lung  symptoms  in  Case  2 ; and  (3)  the  occurrence  at 
one  period  in  Case  4 of  thrombotic  lung  symptoms  indepen- 
dently of  any  recent  superficial  phlebitis.  In  case  5 there 
were  symptoms  of  pulmonary  thrombophlebitis  without 
any  superficial  lesion,  but  there  may  have  been  abdominal 
thromboses.  In  the  case  described  by  Carey  Coombs  the 


356  THROMBOPHLEBITIS  MIGRANS 

because  there  is  no  associated  septicaemia.  The  pulmonary 
thromboses  may  be  heralded  by  agonizing  bouts  of  spas* 
modic  pain  or  by  ordinary  pleuritic  symptoms  which  precede 
haemoptysis,  when  it  occurs,  by  hours  or  days.  The  associa- 
tion of  pleurisy  and  haemoptysis  may  lead  to  an  erroneous 
diagnosis  of  tubercle.  A faintly  turbid  and  blood-stained 
pleuritic  effusion  sometimes  follows.  The  abdominal  throm- 
boses are  characterized  by  pain  and  distension  and  occa- 
sionally (vide  Moorhead  and  Abrahamson)  by  melaena. 
The  symptoms  of  the  cardiac  and  cerebral  thromboses  do 
not  differ  from  similar  lesions  of  other  causation,  but,  as 
small  veins  rather  than  arteries  are  probably  involved, 
prognosis  again  need  not  necessarily  be  regarded  as  un- 
favourable. Treatment  is  expectant  and  symptomatic. 
Liberal  fluids  and  potassium  citrate  may  reasonably  be 
prescribed.  Obvious  focal  infections  should  receive  atten- 
tion at  the  proper  time.  Where  the  gouty  diathesis  is 
present,  or  may  be  presumed,  a purine-free  diet  and  a 
liberal  fluid  intake  should  be  prescribed.  Perhaps  the  most 
important  single  conclusion  to  be  drawn  from  a study  of 
these  cases  is  that  thrombophlebitis  of  this  type  is  to  be 
remembered  as  an  occasional  cause  of  cerebral,  cardiac, 
pulmonary,  and  abdominal  accidents  which  might  other- 
wise prove  difficult  to  explain. 

REFERENCES 

1.  Paget,  J.:  St.  Bartholomew's  IIosp.  Rep.,  I860,  ii.  82. 

2.  Moorhead,  T.  G.,  and  Abrahamson,  L.:  Brit.  Med.  Joum.,  1028, 

i.  586. 

3.  Campbell,  J.  31.  II.,  and  Mono  an,  O.  G.:  Guy's  IIosp.  Rep.,  1930, 

lxn.  34. 

4.  Coombs,  C.  F.:  Quart.  Joum.  Med.  Oxford,  1020-30,  xxiii.  233. 

5.  Briggs,  J.  B.:  Johns  Hopkins  Hosp.  Bull.,  1005,  xvi.  228. 

6.  Heriuck,  W.  W.s  Amer.  Joum.  Med.  Sci.,  1011,  cxlii.  874. 

7 & 8.  Owen,  A.  \Y. : Brit.  Med.  Joum.,  1028,  i.  600 ; and  Bristol  Med. 
Chir.  Joum.,  1030,  xlvii.  20. 

9.  BoEEGcn,  L.:  The  Circulatory  Disturbances  of  the  Extremities. 
Philadelphia  and  London,  1024,  p.  279. 


XXVIII 

NOTES  ON  PROSTATIC  AND  GASTRIC  URAEMIA1 

Tim  uraemia  which  accompanies  primary  renal  disease 
(chronic  interstitial  nephritis)  is  generally  accepted  ns  pro* 
gressive  and  incurable.  There  nrc  two  varieties  of  chronic 
uraemia-  dependent  upon  disease  remote  from  the  kidneys 
which,  if  diagnosed  in  time,  nrc  susceptible  of  cure.  For 
brevity  they  may  be  described  ns  prostntic  nnd  gastric 
uroemin.  At  present  lives  are  lost  through  unfnmiliarity 
with  the  clinical  pictures  presented  by  these  disorders. 
Their  pathologies  arc  entirely  distinct. 

Prostatic  Uraemia 

The  majority  of  patients  suffering  from  the  effects  of 
prostatic  obstruction  find  their  way  to  the  surgeon.  Some  of 
them  show,  in  Addition  to  the  bladder  symptoms,  ns  is  now 
Well  known,  secondary  symptoms  due  to  infection,  or  to 
renal  embarrassment  from  ‘back -pressure’,  or  to  some  com- 
bination of  these.  There  is,  however,  a smaller  group  of 
cases  in  which  the  general  symptoms  due  to  renal  embar- 
rassment so  Tar  outweigh  the  local  symptoms  in  the  minds 
both  of  patient  and  doctor  that  the  advice  of  a physician 
rather  than  ft  surgeon  is  sought.  Retween  May  2031  and 
January  1035  0 eases  of  prostatic  uraemia  have  been  re- 
ferred to  me  by  six  medical  men  of  wide  experience,  nnd 
in  each  ease  without  the  true  state  of  affairs  having  been 
recognized.  In  all  of  them  the  subjective  symptoms  and 
objective  findings  were,  in  fact,  sufficient  for  n diagnosis  of 
uraemia  without  recourse  to  laboratory  tests.  I therefore 
concluded  that  the  clinical  picture  of  uraemia  occurring  in 
the  absence  of  gross  abnormalities  in  the  urine  was  not 
sufficiently  defined  or  appreciated,  nnd  that  a brief  analysis 
of  these  cases  might  be  ns  useful  to  others  ns  it  has  l>een 

* Mnerf.  1K»,  L IPS. 

* The  acute  uracmtii  acenmpanylnjt  pMtrio  Uirmonhag*,  kvttc  d*-- 
lij\Sr»tk>n,  &c.,  art  not  here  under  dbcirnkm. 


358  NOTES  ON  PROSTATIC  AND  GASTRIC  URAEMIA 
instructive  to  me.  One  patient  was  referred  for  ‘anaemia, 
? due  to  a growth* ; a second  for  a bitter  complaint  of  ‘dry 
and  sticky  mouth’;  a third  because  he  looked  too  ill  to 
warrant  some  dental  extractions  advised  on  account  of  back 
pains  which  were  probably  a manifestation  of  his  secondary 
renal  disease.  In  one  only  had  the  prostatic  obstruction 
evoked  comment,  but  not  so  its  relation  to  the  general  symp- 
toms. In  2 cases  an  X-ray  examination  of  the  alimentary 
tract  had  been  carried  out  in  the  hope  of  finding  an  answer 
to  the  general  and  digestive  disturbances.  In  one  of  these 
the  radiologist  had  reported  (three  months  before  the 
patient  came  to  me)  that  the  transverse  colon  was  ‘ elevated 
by  a large  cystic  swelling*.  This  was  the  bladder. 

The  main  clinical  features  of  these  G cases  are  recorded 
in  the  Table  on  p.  3G2.  The  ages  of  the  patients  ranged 
between  56  and  75  years;  the  duration  of  the  uraemic 
symptoms  from  ‘a  few  weeks’  to  six  months.  Symptoms 
referable  to  the  bladder  had  been  present  fora  longer  period. 
None  of  the  patients  included  his  urinary  troubles  among  his 
leading  symptoms.  They  were  either  mentioned  as  an  after- 
thought or  admitted  only  after  direct  interrogation.  Never- 
theless there  was  a palpable  enlargement  of  the  bladder  in 
5 of  the  G cases,  and  frequency  was  present  in  every  case 
but  one.  In  1 case  there  was  no  albumin  in  the  urine ; in  the 
remainder  ‘a  trace’  only.  The  specific  gravity,  when  re- 
corded, ranged  between  1005  and  1008.  In  1 case  there 
was  a gross  pyuria,  and  in  2 ‘a  few  pus  cells’  were  noted 
in  the  centrifugalized  deposit.  In  the  remainder  there  were 
either  no  cells  or  the  specimen  was  perfectly  clear  to  the 
naked  eye.  In  no  case  was  peripheral  oedema  or  retinitis 
observed.  The  blood-pressure  readings  varied  between 
140-90  and  190-125. 

Subjective  symptoms. — Loss  of  appetite  was  constant  and 
sometimes  pronounced  and  was  once  associated  with  a dis- 
inclination for  tobacco.  Thirst  was  pronounced  in  4 of  the 
G cases.  A ‘nasty’  and  a ‘salty’  taste  in  the  mouth  and  a 
‘dry,  sticky  mouth’  were  specifically  complained  of  by  three 
patients.  Weakness  and  languor  were  twice  remarked  upon 
and  diurnal  drowsiness  once.  Pruritus,  nausea,  headache. 


NOTES  ON*  PROSTATIC  AND  GASTRIC  URAEMIA  35t» 
dyspnoea  on  effort,  cramps,  and  pains  in  back  and  limbs 
each  received  a single  mention.  Some  degree  of  malaise  is 
usual  and  impairment  of  mental  efficiency  and  character 
changes  may  be  noticed  by  relatives.  George  Moore  in  the 
dedication  of  his  last  novel  to  Sir  John  Thomson-Walker 
tvas  eloquent  in  Ids  description  of  his  own  failure  of  mental 
power  prior  to  his  operation.  After  the  operation  he  re- 
covered all  his  old  literary  ability.  Any  or  all  of  the  symptoms 
described  above  would  be  considered  usual  in  the  presence 
of  gross  nephritic  manifestations,  ora  markedly  albuminous 
urine.  It  is  in  the  nbscncc  of  these  thnt  they  tend  to  mislead. 

Objective  manifestations. — There  was  loss  of  weight  in 
every  case — in  1 ease  ‘nearly  a stone  in  4 cases  half  a stone 
or  over;  in  1 ease  4 pounds.  All  of  the  patients  looked  ‘off 
colour’;  0 showed  the  slight  earthy-brown  tint  common  to 
other  types  of  uraemic  disease.  A dry  tongue  is  common. 
The  curious  ‘fishy*  odour  in  the  breath,  which  has  on  other 
occasions  helped  me  to  the  diagnosis  of  uraemia,  was  noted 
in  3 eases,  and  in  one  of  these  had  been  remarked  by  the 
patient  and  bis  wife.  Haemoglobin  estimations  were  made 
in  4 eases,  the  readings  being  48,  CO,  G5,  and  70  per  cent. 
The  blood-urea  figures  ranged  from  107  mg.  per  100  c.cm. 
to  288  mg.  per  100  c.cm.  In  the  ease  of  No.  2 the  reliability 
of  the  urea  estimation  by  a technical  assistant  was  called 
in  question.  This  patient  made  a full  recover)'  after  a 
two-stage  prostatectomy.  There  was  no  close  correlation 
between  the  height  of  the  urea  figures  and  the  clinical 
symptoms  or  signs,  with  this  exception  that  the  case  with 
the  highest  figures  presented  the  lowest  haemoglobin  and 
was  the  only  one  in  which  vomiting  was  mentioned.  The 
'fishy*  breath  was  recorded  in  the  eases  with  the  highest 
and  the  two  lowest  readings.  In  No.  3 the  salivary  urea 
was  estimated  on  account  of  the  unpleasant  * metallic  * 
taste  compfafnetf  of,  and  gave  a figure  of  C 2 mg.  per 
100  c.cm.  as  compared  with  a blood' urea  of  07  mg. 

Although  the  blood -pressure  was  high  in  5 out  of  the  fi 
raves  there  nas  no  rravon  to  suspect  the  simultaneous 
presence  of  primary  renal  disease,  the  age  and  earlier  history 
of  the  patients,  the  absence  of  retinitis,  and  the  rmall  traces 


360  NOTES  ON  PROSTATIC  AND  GASTRIC  URAEMIA 
of  albumin  furnishing  the  chief  arguments  against  this  pos- 
sibility. 

In  no  case  was  there  any  account  of  convulsions.  One 
case  is  well  after  a two-stage  operation.  Two  were  well 
some  months  after  the  first  operation.  Two  have  not  been 
reported.  One  case  died  in  coma  after  a first-stage  operation. 
Wc  now  believe,  from  the  observations  of  D.  McAlpine1  and 
others,  that  the  convulsive  phenomena  of  chronic  nephritis 
are  generally  expressive  not  of  the  intoxication  but  of  the 
accompanying  hyperpiesia  and  hypcrpietic  crises  of  arterial 
disease.  They  can  occur  in  cases  of  hyperpiesia  with  normal 
renal  function.  Conversely  cases  of  prostatic  and  gastric 
uraemia,  although  cramps,  muscular  twitchings,  and  coma 
may  supervene,  seem  little  liable  to  convulsion.  Once  more 
it  should  be  emphasized,  for  it  helped  to  explain  why  they 
escaped  diagnosis,  that  for  the  most  part  these  six  patients 
thought  that  they  were  passing  plenty  of  urine.  They  may 
indeed  pass  plentiful,  dilute  water.  As  they  were  troubled 
with  frequency,  it  had  not,  with  one  exception,  occurred  to 
them  that  micturition  was  seriously  obstructed  or  that  they 
were  suffering  from  actual  retention.  This  lack  of  apprecia- 
tion may  be  due  in  part  to  the  fact  that  when  a hollow 
organ  becomes  gradually  and  grossly  distended  it  is  less  able 
to  register  discomforts,  and  in  part,  perhaps,  to  the  ‘dulling’ 
of  perception  which  is  a feature  of  the  uraemic  state. 

The  following  case  is  particularly  instructive  as  the 
patient,  although  more  gravely  ill  than  the  others,  had 
noticed  no  urinary  symptoms  excepting  that  he  had  to 
pass  water  once  at  night. 

Case  5.  Male,  aged  G7,  complained  of  recurring  attacks  of  nausea 
and  vomiting  during  the  past  G months.  lie  experienced  no  abdo- 
minal pain  at  any  time.  He  had  had  an  X-ray  examination  of  his 
alimentary  tract  3 months  previously.  He  and  his  wife  had  noticed  a 
curious,  unpleasant  odour  in  the  breath.  He  had  been  troubled  with 
fidgets  and  cramps.  He  had  lost  half  a stone  in  weight,  and  there  was 
noticeable  wasting  about  the  shoulders.  The  bladder  was  distended 
to  the  navel.  Prostate  much  enlarged,  nis  blood-pressure  was  195- 
110.  Haemoglobin  43  per  cent.  Urine  clear,  specific  gravity  1003, 
no  albumin  or  sugar.  A few  leucocytes  but  no  casts  in  the  eentri- 

1 Quart.  Joum.  of  Med.,  1933,  xxvi  4G3. 


NOTES  ON  PROSTATIC  AND  GASTRIC  URAEMIA  SGI 
fugnlized  deposit.  Urine  urra  0 83  per  cent.  niood-urea  288  mg.  per 
IOO  e.cm.  After  11  months  of  suprapubic  drainage  this  patient  has 
recovered  his  w ell-bclng, Ms  weight  has  risen  by  1 it.,  the  haemoglobin 
fs  new  80  per  cent.,  and  the  blood  pressure  2G0-Z 10.  The  blood-urea, 
however,  is  still  110  mg.  per  100  c.cm. 

The  differential  diagnosis  of  prostntic  uraemia  in  the 
ambulator)’  phase  is  from  abdominal  malignant  disease  and 
other  causes  of  anaemia  and  anorexia  appropriate  to  the 
sixth  and  seventh  decades. 

Gasthic  Uraemia 

Tins  condition  is  associated  with  other  biochemical  dis- 
turbances besides  nitrogen  retention — namely,  an  alkalosis 
and  a chloride  deficiency.  It  may  result  from  gastric  or 
duodcnnl  ulceration,  generally  but  not  always  complicated 
by  some  degree  of  stenosis;  from  pyloric  obstruction  due 
to  new  growth;  and  from  a high  intestinal  obstruction. 
Repented  vomiting,  vigorous  alkaline  therapy  (particu- 
larly in  the  presence  of  pyloric  stenosis  or  any  associated 
renal  inadequacy),  and  gastric  hnemorrhage  all  tend  to 
encourage  alkalosis  and  uraemia.  A raised  blood-urea, 
from  twice  to  five  times  the  normal  figure,  may  nlso  be 
found  in  cases  of  pyloric  stenosis  when  clinical  symptoms 
of  uraemia  arc  absent.  I have  now  made  it  a routine  to  nsk 
for  a blood-urea  estimation  in  all  eases  of  pyloric  narrowing* 
whether  Ijcnign  or  malignant,  as  n high  figure  calls  for 
social  care  in  respect  of  pre-  and  post-operative  treatment 
and  anaesthesia. 

A valuable  group  of  papers1  on  alknlnexnia  and  renal 
insufficiency  in  gastric  disease  by  Hurst,  Wynn  Houghton, 
Venables,  and  Lloyd  appeared  in  the  Guy'*  Hospital  Re- 
port* in  1025,  together  with  references  to  the  English  and 
American  literature.  Cooke*  lmv  carefully  studied  the  alka- 
losis accompanying  the  alkaline  treatment  of  peptic  ulcer. 
M,  Rnehmilewitx*  has  nho  discussed  the  gastric  and  other 
causes  of  *cxtrarennl  a7otaernia  *. 

* Vuy't  limp,  ftrporU,  lies,  JITU  »*■*}. 

* Cool*.  A. *1.  Jtnm.  «/ Jfot,  IW,  Xivi.  377. 

* tjxitxi,  mi.  i,  r>. 


NOTES  ON  mOSTATIC  AND  GASTRIC  URAEMIA  863 

Among  10  oases  of  gastric  uraemia  in  rny  own  practice 
there  were  fi  eases  of  duodenal  tilccr,  1 of  gastric  ulcer 
(prepyloric),  and  3 cases  of  pyloric  carcinoma.  Only  one 
of  these  had  been  subjected  to  intensive  nlkalinc  therapy 
before  the  onset  of  uraemic  symptoms.  Vomiting  had  been 
severe  before  the  onset  of  symptoms  in  4 cases,  slight  in  4, 
nnd  absent  in  1 — the  ease  receiving  nlkalinc  therapy.  Two 
cases  had  slight  nnd  1 severe  bleeding  at  the  time  of  develop- 
ment of  the  uraemic  symptoms,  or,  conversely,  bleeding  may 
have  occurred  in  concert  with  the  uraemia.  Three  cases  with 
duodenal  ulceration  recovered  after  operation.  One  ease  of 
pyloric  carcinoma  survived  the  relieving gostro -enterostomy 
with  immediate  benefit.  The  remainder  died. 

The  symptoms  recorded  in  this  group  included  mental 
disturbance,  drowsiness,  headache,  thirst,  hiccups,  muscu- 
lar twitching,  stupor,  nnd  coma,  Anorexia,  irritability, 
apathy,  nnd  pruritus  have  also  been  recorded  by  others  as 
premonitory  of  graver  trouble.  ‘Fishy’  breath  nnd  earthy 
pigmentation  of  the  face  were  striking  features  in  one  case 
to  be  described  later.  The  blood-urea  figures  in  my  own 
series  have  ranged  from  twice  to  seven  times  normal. 

Cases  illustrative  of  various  events  arc  described  here- 
under. 

Cask  1.  Gastric  utter  with  fatal  alkalosis  and  uroemta. — Female, 
aged  50.  Tills  patient,  whose  ca«o  was  previously  rej>ortetl  by  Wynn 
Houghton,  vm  admitted  to  hospital  for  vomiting,  without  pain.  She 
wni  found  to  have  8 hours’  pi&tric  stasis  by  the  barium  meal  but  with- 
out a visible  lesion ; she  vrns  promptly  relieved  by  gastric  Lavage.  She 
was  readmitted  later  wills  a return  of  symptoms,  Ixmme  mentally 
peculiar  nnd  emotional,  and  finally  jtuporose,  and  died.  The  blood- 
urea  was  two  nnd  a lalf  limes  normal.  There  was  no  albuminuria  at 
find,  but  albumin  and  easts  apj>earrd  shortly  before  death.  At  the 
autopsy  a prepyloric  ulcer,  which  was  not  eneroftchlng  upon  the 
sphincter,  ami  a mild  gastritis  were  the  only  pathological  findings. 
The  kidneys  were  normal  to  naked -eye  Inspection. 

Cask  2.  Duodenal  uUrr  with  stenosis;  all  ale,  sis  and  uraemia  immedi- 
ately foihr.dng  g-tstro-Jejunoitomy;  rranery. — Male,  aged  St.  Dave  a 
20  years’  history  of  dyspepsia.  Fight  years  previously  he  had  been 
operated  on  for  « {■erforaled  duodenal  ulcer.  Two  years  brforr  be  sat 
referred  to  me  by  Dr.  Tlemard  Ilalgh  l»e  started  alkaline  treatment, 
taking  a quarter  of  a |>ound  of  Maclean’*  powder  each  week.  Decently 


304  NOTES  ON  PROSTATIC  AND  GASTRIC  URAEMIA 
he  had  complained  of  copious  acid  vomits  and  had  lost  nearly  2 st.  in 
weight.  There  was  visible  peristalsis.  In  addition  he  showed  slight 
hyperthyroid  symptoms  and  a blood-pressure  of  200-120.  He  was 
admitted  to  Guy's  Hospital,  where  the  diagnosis  of  pyloric  stenosis 
from  a chronic  duodenal  ulcer  was  confirmed.  Mr.  Pliilip  Turner 
operated,  performing  a short  circuit.  Shortly  after  coming  round  from 
the  anaesthetic  he  became  restless  nnd  mentally  peculiar,  and  finally 
stuporose.  However,  with  salines  and  sedatives  fie  recovered.  The 
blood-urea  was  112  mg.  per  100  c.cm.  He  liad  not  been  haring  inten- 
sive alkaline  therapy  before  the  operation,  nor  bad  he  complained  of 
general  symptoms,  or  been  noticed  to  be  peculiar  in  any  way.  With 
a blood-urea  estimation  prior  to  operation  it  is  possible  that  tliis 
anxious  episode  might  have  been  avoided. 

Case  3.  Duodenal  ulcer  without  gastric  stasis;  alkalosis  and  uraemia 
following  all; aline  therapy;  recovery;  gastro-jejunostomy. — Male,  aged 
43.  Had  suffered  in  earlier  life  from  bilharzia  and  pulmonary  tuber- 
culosis. Intermittently  over  a period  of  C years  be  had  been  troubled 
with  symptoms  of  duodenal  ulcer,  usually  responding  promptly  to 
diet  and  strict  treatment.  In  June  1033  he  had  a vomiting  attack 
with  a slight  hacmatcmcsis.  He  then  remained  fairly  well  until  the 
beginning  of  December  1033,  when  he  had  another  small  haemate- 
mesis.  He  was  put  to  bed  and  given  frequent  doses  of  Maclean’s 
powder.  I saw  him  on  11  December  when  he  was  looking  very  111, 
drowsy,  apathetic,  with  a brown-tinted  complexion,  dry  tongue,  nnd 
‘fishy’  breath.  He  was  admitted  to  a nursing-home  where  he  re- 
mained very  drowsy  for  some  days.  He  complained  of  slight  headache 
and  had  to  be  roused  to  talk  or  to  take  his  feeds.  There  was  pro- 
nounced thirst.  Urine  plentiful,  with  only  a haze  of  albumin,  prob- 
ably due  to  a chronic  cystitis  with  pyuria.  Previously  his  renal  func- 
tion was  known  to  be  satisfactory.  Blood-pressure  140-00.  Alkalis 
were  immediately  stopped.  The  blood-urea  figure  was  175  mg.  per 
100  c.cm.  He  slowly  improved.  After  0 weeks  the  blood-urea  liad 
fallen  to  5S  mg.  per  c.c.,  but  gastric  symptoms  bad  again  become 
troublesome  and  feeding  was  difficult.  No  gastric  stasis  was  demon- 
strable radiologieally.  After  preparation  with  continuous  intravenous 
saline  a gastro-jejunostomy  was  performed  by  3Ir.  L.  Bromley  in 
February  1934.  Convalescence  was  slow  but  immediate  recovery 
complete.  Later  recurrences  of  gastric  symptoms  with  perforation 
led  to  further  surgery  and  ultimately  to  a partial  gastrectomy. 

Case  4.  A man,  aged  68  years,  had  been  troubled  for  upwards  of 
20  years  with  gastric  symptoms  of  which  vomiting,  coming  in  attacks 
but  with  free  intervals,  had  been  the  outstanding  symptom.  Gastric 
stasis  up  to  9 hours , as  shown  with  the  barium  meal,  had  been  reported 
a year  previously  and  a test-meal  had  shown  hypersecretion.  Opera- 
tion had  been  declined.  I saw  him  with  Dr.  Allen  on  4 February  1035. 


NOTES  ON*  PROSTATIC  AND  GASTRIC  URAEMIA  SOS 
A week  previously  he  had  had  n vomiting  attack  and  was  given 
alkali*  but  not  in  large  doses.  On  31  January  the  vomiting  had stopped 
but  he  felt  ill  In  himself.  In  the  4$  hours  preceding  the  consultation 
he  had  l>ccome  drowsy  nnd  thirsty  with  a dry  tongue  and  slight 
twitching  of  the  limbs.  He  was  just  able  to  answer  questions,  but 
was  very  confused.  There  was  no  visible  dilatation  of  the  stomach,  no 
peristalsis  or  splash,  but  I noted  marked  resistance  in  the  right  upper 
quadrant.  The  urine  showed  a very  slight  hare  of  albumin ; no  cast*. 
Thr  blood-urea  was  1 19  rog.,  but  the  urine  contained  3 per  cent,  of 
urea.  A diagnosis  of  pyloric  stenosis  from  an  old  duodenal  ulcer  srith 
‘gastric  uraemia*  seas  made.  It  svas  decided,  in  consultation  with 
I.ord  Ilorder  and  Mr.  IV.  II.  Ogilsie,  that  in  his  present  state  opera- 
tion was  out  of  the  question.  His  stomach  svas  stashed  out  and  he 
stas  given  continuous  intravenous  glucose-saline,  taking  approxi- 
mately 10  pints  in  -W  hours.  His  subsequent  blood -urea  figures  svere 
as  follows; 

0.2.35  . . . .75  mg. 

0.2.35  . . . .05  mg. 

13.2.33  . . . .CO  mg. 

18.2.35  . . , .55  mg. 

20.2.35  . . . .50  mg. 

After  the  first  few  das'*  fluid  moulh-feeding,  srithout  alkalis,  svas 
re  instituted.  On  18  February  vomiting  started  again.  On  10  February 
gastric  lavage  brought  away  450  c.e.  of  dark  bihous  fluid.  On  20 
February,  under  morphine  and  splanchnic  block  anaesthesia,  Mr. 
Ogilvic  operated.  He  found  a large  inflammatory  mass  !>enrath 
the  liver  nnd  involving  the  duodenum  and  performed  a gastro-entrr- 
ostomy.  The  patient  made  a good  recovery  and  left  the  nursing- 
home  on  a light  mixed  dietary  on  20  March  1035.  Ilis  Last  blood -urea 
figure,  on  5 .March,  was  4!>  mg. 

Whatever  part  the  associated  alkalosis  nnd  chloride  defi- 
ciency mny  play  in  these  cases  it  will  l>c  seen  that  the  clinical 
picture  of  gastric  uraemia  includes  symptoms  common  to 
nephritic  nnd  pros  f a tie  uraemia.  These  common  symptoms 
mny  indeed  l>c  regarded  as  the  true  .symptoms  of  uraemia, 
1 have  not  cncomitrrrd  any  case  of  gastric  uraemia  srith 
convulsion.  Tetany,  which  was  formerly  regarded  as  an  im- 
portant nervous  manifestation  of  pyloric  olwtruction,  has 
not,  so  far  ns  1 can  recollect,  been  record ed  among  any  of 
my  private  or  hospital  cases  of  ulcer  or  cancer  in  rrernt 
yrar*.  Seen  in  the  stagr  of  coma  with  a normal  urine  nnd 
an  indefinite  gastric  history  the  diagnosis  of  gastric  uraemia 
may  present  great  difficulties. 


366  NOTES  ON  PROSTATIC  AND  GASTRIC  URAEMIA 
Treatment 

The  treatment  of  prostatic  uraemia  is  mainly  a matter  for 
the  surgeon.  It  includes  careful  'decompression’  of  the  dis- 
tended bladder,  a two-stage  operation,  and  treatment  of 
the  anaemia. 

The  treatment  of  gastric  uraemia  includes  the  prompt 
withdrawal  of  all  alkalis,  gastric  lavage,  rectal  salines,  and, 
in  grave  cases,  or  as  preparation  for  operation  in  cases  with 
a high  blood-urea,  intravenous  salines  by  the  continuous 
method,  and  finally  appropriate  surgery,  With  extension  of 
the  knowledge  that  uraemia  may  be  due  to  extrarenal 
causes,  prostatic  and  gastric  uraemia  should  commonly  be 
preventable. 


XXIX 


MYXOEDEMA  AND  OTHER  MANIFESTATIONS  OF 
THYROID  DEFICIENCY1 

Ik  the  case  of  the  patient  whom  I bring  before  you  I will 
reverse  the  usual  order  of  procedure,  nnd  before  considering 
her  history  nnd  symptoms,  ask  your  attention  to  certain 
physical  features,  nnd  particularly  to  her  facial  appearance. 
Physiognomical  diagnosis  is  nn  important  chapter  in  clinical 
medicine,  nnd  liccomes  steadily  more  so  ns  wc  turn  the 
pages  of  experience.  There  nrc  few  cases  in  which  the  face 
will  tell  us  nothing.  There  nrc  some  in  which  it  tells  us 
almost  everything  wc  need  to  know.  In  acromegaly,  myxoe- 
demn,  Graves’s  disease,  in  some  cases  of  tabes  dorsalis,  in 
the  Parkinson’s  mask  of  paralysis  ngitans  nnd  encephalitis 
lctlmrgicn,  in  pernicious  nnaernia,  in  the  Hippocratic  facies 
of  grave  abdominal  disease,  and  in  the  mitral  facies  wc  have 
well-known  examples  of  ‘diagnostic  physiognomies’,  and 
the  list  might  be  considerably  extended.  Not  infrequently 
the  countenance  of  disease  will  guide  us  to  n correct  opinion 
when  the  physical  overhaul  or  the  talc  of  symptoms  is  un- 
convincing. In  cxnmining  facial  characters  wc  take  into 
account  the  general  conformation  nnd  proportions,  the 
colouring  nnd  nutrition,  the  texture  of  the  skin,  the  expres- 
sion, nnd  the  distribution  of  the  hair,  any  or  all  of  which 
may  show  some  significant  change. 

You  will  doubtless  be  chiefly  impressed  by  the  anaemic 
appearance  of  this  patient,  hut  note  how  broad  her  features 
ore,  how  placid  and  immobile  and  lacking  in  any  play  of 
emotion.  Although  there  is  n marked  underlying  pallor, 
with  a slightly  yellow  tint,  the  cheeks  arc  peculiarly  pink. 
The  skin  is  smooth,  like  china.  The  eyebrows  are  scanty, 
and  the  hair-nmrgm  has  so  far  receded  towards  the  vertex 
that  she  lias  found  it  necessary  to  arrange  her  coiffure  so  as 
to  hide  this  deficiency.  When  I try  to  pluck  tip  the  skin  of 

* Cuy't  Uaty.  CsutU,  UCO,  afcy.  lii. 


308  MYXOEDEMA  AND  OTHER 

the  forehead  I find  this  almost  impossible  on  account  of  the 
thickness  of  the  skin,  and  on  taking  the  tissues  of  her  cheeks 
between  o finger  and  thumb  a feeling  as  of  some  firm  infiltra- 
tion is  imparted.  These  are  the  facial  characters  of  myxoe- 
dema,  and  although  in  her  case  there  arc  some  additional 
findings,  including  a large  spleen,  which  have  suggested  the 
possibility  of  a mixed  pathology,  they  justify,  when  taken 
in  conjunction  with  her  own  complaints,  a fairly  confident 
diagnosis. 

Our  patient  is  aged  42  and  married.  She  has  had  5 chil- 
dren and  2 miscarriages.  Fifteen  months  ago  she  noticed 
that  she  was  getting  pale,  and  since  then  there  has  been  in- 
creasing loss  of  energy  and  dyspnoea  on  exertion.  Her  hair 
has  been  getting  thinner.  She  does  not  sweat  as  readily  as  she 
used  to  do.  She  prefers  the  warm  weather.  Her  weight  lias 
not  altered  appreciably.  In  the  ward  we  have  been  struck 
by  her  slow  speech  and  her  impassive  behaviour.  Her  voice 
is  husky  at  times.  She  has  a broad  and  rather  smooth 
tongue,  and  on  account  of  this  smoothness  and  her  anaemia 
and  the  enlargement  of  the  spleen  the  possibility  of  perni- 
cious anaemia  had  been  discussed.  However,  the  blood 
count  shows  a microcytic  anaemia,  with  haemoglobin  down 
to  25  per  cent,  and  a colour-index  of  0-3.  She  does  not  show 
the  slowing  of  the  pulse  and  markedly  subnormal  tempera- 
ture frequently  manifest  in  myxoedema. 

Before  passing  to  a more  general  discussion  of  the  disease 
and  its  differential  diagnosis  and  treatment,  I should  like 
you  to  listen  to  the  histories  of  two  other  patients.  In  these 
cases  the  diagnosis  was  further  confirmed  by  the  response  to 
treatment — a confirmation  which  we  have  still  to  obtain  in 
the  case  before  us. 

Case  1.  Mrs.  N — , aged  42,  was  admitted  on  23  February  1023. 
Her  mother  died  of  consumption.  She  had  two  daughters  living, 
aged  21  and  19  years.  Two  other  children  died  in  infancy.  Twenty- 
two  years  ago  she  had  enteric  fever.  Before  this  date  she  enjoyed  per- 
fectly good  health,  hut  she  has  never  felt  really  fit  since  the  illness. 
In  1011  she  had  pneumonia,  and  six  months  later  was  operated  on  for 
appendicular  abscess.  These  two  illnesses  further  aggravated  her 
feelings  of  unfitness.  For  12  years  she  has  noticed  gradually  increasing 
muscular  weakness,  with  impairment  of  memory  and  slowness  of 


MANIFESTATIONS  OF  THYROID  DKITCIKSCCY  5C9 
ipwh.  She  hat  alto  experienced  on  Increasing  intolerance  for  coM, 
and  feels  chilly  cv  en  in  summer.  In  recent  years  she  lias  been  growing 
fat,  though  latterly  she  hat  again  lost  weight.  She  lias  noticed  puffi- 
ness  of  the  face  and  eyelids  and  dryness  of  the  skin.  She  never  sweats. 
Recently  she  has  had  to  give  up  her  household  duties  on  account  of 
weakness.  She  frequently  forgets  what  she  wants  to  say,  and  whereat 
she  used  to  tie  ‘sharp-spoken’,  she  It  now  ‘very  slow'.  Her  Itair  hat 
been  falling.  The  period*  have  hem  Irregular.  She  wat  tent  to  Kuy'*, 
however,  not  so  much  for  these  genera!  symptoms  at  for  some  vague 
abdominal  discomforts,  for  which  she  was  seen  by  Mr.  Turner,  lie 
considered  that  these  symptoms  could  be  sudlriently  accounted  for 
by  visceroptosis,  and  was  struck  by  her  general  condition.  He  drew 
attention  to  the  hypcracmic  patches  on  her  cheeks,  which  suggested 
mitral  stenosis.  These  were  a striking  feature,  contrasting  sharply 
with  her  rather  yellowish  underlying  paJJor.  Kvrn  more  striking, 
however,  was  the  general  heaviness  of  the  features,  nnd  the  complete 
absence  of  any  play  of  emotion  or  expression  In  the  course  of  the 
Interrogation.  The  eyelids  were  slightly  puffy.  The  lialr  was  dry  and 
coarse,  nnd  the  outer  half  of  the  eyebrows  was  lacking;  the  hair- 
mnrglnluidcoasidcrahly  receded.  Her  voice  was  monotonous,  and  her 
words  were  uttered  slowly.  Her  latent  period  In  answering  questions 
was  longer  than  normal.  The  Integument  of  the  forehead  was  thick. 
The  skin  was  everywhere  dry,  nnd  the  axillary  hair  was  scanty. 
Her  puta  was  fit,  temjK-raturr  07-4®,  nnd  respiration -rote  20.  The 
systolic  blood-prrssurr  was  105.  The  blood  showed  a haemoglobin 
pererntage  of  05,  and  n ml  cell  count  of  4.140,000.  The  1kjs.i1  mrta- 
bolle  rate  was  minus  21-7  per  cent.  Ohicose  tolerance  wns,  however, 
normal.  It  should  be  mentioned  tliat  she  had  l>cen  taking  small  doses 
of  thyroid  while  awaiting  admission.  She  was  treated  with  thyroid  In 
the  form  of  Tab.  Thyroid  (It,  & \V,J,  and  seemed  to  do  best  on  a dose 
of  gr.  2 thrice  dally,  lids  represents  only  nlmut  gr.  1 1 of  dried  thyroid 
in  the  day.  Shr  improved  ttrndily,  nnd  a few  months  later,  excepting 
for  a slight  tendency  to  diulnras,  had  lost  all  her  symptoms,  llrr 
colour  had  Improved  remarkably.  In  figure  she  became  slim  and 
sprightly.  Her  fare  and  expression  were  happy  nnd  vivacious. 

Cask  2.  Mr.  M— , aged  about  50,  was  admitted  on  SO  April  1023. 
He  complained  of  ‘debility  and  noises  In  the  head*.  In  1011  l»e  l*e- 
came  gradually  weak  In  his  legs  ami  arms,  nnd  after  the  sligMrvt 
exertion  he  fell  exhausted  and  t/m f.  7n  19 19  hr  felt  mu<h  «nd 

wns  admitted  to  £t.  JlarUndoroew'*  Hospital.  He  toys  that  hr  was 
treated  there  for  ‘septic  anaemia  nnd  liver  trouble*  for  which  hU 
teeth  were  extracted.  He  has,  however,  remained  (nna;>abte  of  any 
sustained  effort;  has  felt  the  cold  severely;  Id*  I save  been 

essnt/jmted,  and  lie  hs*  continually  felt  ml  *r»f  tired,  latterly  M* 
memory  Ita*  twen  defective. 

He  looked  very  different  from  the  patient  juit  described,  and  jet 


370  MYXOEDEMA  AND  OTHER 

Ins  appearance  at  once  surest ed  myxoedema.  He  was  not  fat,  and 
did  not  show  the  patch  of  malar  hyperaemia ; nevertheless  his  face 
was  expressionless ; his  forehead  was  corrugated  and  stiff,  but  smooth 
and  shiny  between  the  wrinkles ; liis  hair  was  sparse,  and  felt  curiously 
dry  and  coarse  when  rolled  between  the  fingers,  and  was  altogether 
lacking  in  gloss.  His  face  had  a yellowish  tinge ; on  the  trunk  the  skin 
was  scaly  and  dry ; sweating  was  entirely  absent ; the  wrinkled  skin 
of  his  neck  was  reminiscent  of  the  tortoise ; his  speech  and  movements 
were  laborious  and  slow.  The  first  time  we  examined  him  at  the  bed- 
side the  sister  said,  * Would  you  like  to  see  him  take  his  own  shirt  off?  * 
She  had  recognized  that  this  leisurely  act  was  a demonstration  in 
itself.  His  haemoglobin  was  78  per  cent.;  his  red  cells  3,7-10,000. 
His  basal  metabolic  rate  was  nearly  50  per  cent,  below  normal.  Before 
treatment  his  daily  metabolism  amounted  to  only  803  calories.  A 
month  later,  after  treatment  with  Tab.  Thyroid  (B.  & W.)  rising  to 
gr.  8 per  day,  his  daily  metabolism  amounted  to  1,480  calories — still 
a low  figure. 


Aetiology  and  General  Features 

Myxoedema  is  a disease  of  adults,  and  occurs  for  the  most 
part  in  women  shortly  before,  during,  or  after  the  meno- 
pause. Seven  women  are  affected  for  ever}’  one  man.  One- 
half  of  the  cases  occur  between  the  ages  of  30  and  50.  No 
definite  predisposing  factors  are  known,  but  sometimes,  as 
in  Case  2,  the  symptoms  seem  to  have  developed  insidiously 
after  a severe  illness. 

The  symptoms  are  those  which  one  would  expect  from  a 
general  depression  of  metabolism,  but  we  may  go  further 
and  say  that  there  is  no  vital  function  which  may  not  share 
in  the  depression.  Weight  is  frequently,  but  not  always, 
increased ; fatty  pads  may  develop  above  the  clavicles ; the 
pulse  is  slow ; the  temperature  is  subnormal ; the  patients 
nearly  always  complain  that  they  feel  the  cold  much;  the 
skin  is  dry,  the  hair  coarse  and  scanty;  the  eyebrows  are 
commonly  deficient  in  their  outer  half;  the  nails  are  brittle, 
and  the  bowels  costive.  Movements  and  speech  are  slow 
and  lack  expression.  The  voice  may  be  husky,  and  in 
advanced  cases  dwindles  to  a croak,  owing  to  submucous 
infiltration  of  the  vocal  cords.  The  facies  often  betray  the 
diagnosis  directly  the  patient  enters  the  room.  No  emotion 


MANIFESTATIONS  OF  THYROID  DEFICIENCY  371 
seems  to  light  up  the  features  during  conversation,  and  a 
smile,  if  it  appears,  is  sIott  to  develop.  The  face,  contradic- 
tory though  it  may  seem,  is  both  abnormally  smooth  and 
wrinkled.  The  smoothness,  as  depicted  by  Gull,  resembles 
porcelain,  but  around  the  eyes  and  mouth  are  frequently 
to  be  seen  numerous  fine  wrinkles.  The  eyelids  are  thick 
and  puffy  and  look  oedematous,  or  as  though  they  had 
recently  been  oedematous.  Nephritis  may  suggest  itself  at 
the  first  glance,  or  a suspicion  of  mitral  disease  may  be 
entertained  on  account  of  the  peculiar  patch  of  purplish- 
pink  hyperacmia  the  upon  cheeks — ‘ the  cheeks  tinted  of  a 
delicate  rose-purple’  (Gull).  The  hands  are  coarse,  and 
sometimes  referred  to  as  spade-like.  The  legs  may  appear 
infiltrated,  but  unless  the  disease  is  complicated  by  renal 
inefficiency  or  severe  anaemia,  there  is  no  pitting  on  pres- 
sure. The  urine  contains  no  albumin.  There  may  be  a slight 
or  sometimes  a severe  anaemia  of  the  secondary  type — a 
feature  not  always  sufficiently  stressed,  which  led  to  the 
suggestion  that  the  thyroid  gland  might  be  a haemopoietic 
organ.  More  rarely  there  is  a macrocytic  anaemia.  The 
psychology  of  these  cases  no  less  than  their  physique  is 
affected.  In  the  earlier  stages  the  patient  notices  her 
langour  and  disinclination  for  mental  effort  and  concentra- 
tion. Later  this  becomes  obvious  to  all,  and  she  is  heavy 
and  unresponsive  and  her  speech  is  slow  and  toneless. 
The  memory  becomes  poor.  Nothing  is  more  remarkable  in 
the  general  improvement  under  treatment  than  the  return 
of  vivacity,  the  altered  timbre  in  the  voice,  and  the  recovery 
of  mental  alertness  and  elasticity.  Amenorrhoea  is  often 
present  in  cases  developing  prior  to  the  menopause,  although 
sometimes  there  is  irregular  or  excessive  loss.  Menstruation 
may  reappear  under  treatment,  and  it  is  stated  that,  after  a 
period  of  sterility,  fertility  has  been  re-established.  JBy 
estimations  of  the  basal  metabolic  rate  determination  of  the 
degree  of  hypothyroidism  has  become  possible.  But  an 
adequate  estimate  of  this  and  of  improvement  under  treat- 
ment may  be  obtained  by  observations  of  the  general 
symptoms,  pulse  and  respiration  rates,  temperature  curve 
and  weight. 


372 


MYXOEDEMA  AND  OTHER 


Dhterential  Diagnosis 

In  a fully  developed  case  the  diagnosis  of  myxoedema 
should  not  be  difficult,  and  yet  there  are  four  conditions  for 
which  it  is  not  infrequently  mistaken. 

The  first  is  mitral  stenosis  or  other  heart  disease — on 
account  of  the  purplish  malar  hyperaemia.  A woman,  aged 
69,  came  to  see  me,  looking  so  ill  and  sallow  and  with  such  a 
purple  hue  to  her  cheeks  that  I could  well  understand  why 
she  had  been  kept  in  bed  for  some  weeks  as  a case  of  heart 
disease.  Her  complaint  of  great  weakness  and  some  dys- 
pnoea lent  additional  weight  to  the  opinion.  However,  I 
could  find  no  sign  of  cardiovascular  disease,  and  she  showed 
many  other  stigmata  of  myxoedema.  She  was  restored  to 
active  health  by  thyroid  treatment. 

It  should,  however,  be  mentioned  that  a genuine  condi- 
tion of  ‘myxoedema  heart’,  with  myocardial  changes 
clinically  and  cardiographically  manifest,  has  been  de- 
scribed. Dr.  J.  M.  H.  Campbell  gave  a good  account  of  this 
condition  in  the  Guy's  Hospital  Reports  for  1934. 

The  second  is  pernicious  anaemia.  Confusion  occurs, 
first  because  myxoedematous  patients  may  show  a ‘yel- 
lowy* anaemia,  not  unlike  the  lemon  tint  of  the  other 
disease ; secondly,  because  patients  with  pernicious  anaemia 
not  uncommonly  present  a smooth  skin  and  other  facial 
features  a little  suggestive  of  thyroid  deficiency.  Perhaps 
the  activity  of  the  thyroid  gland  is  actually  subnormal  in 
virtue  of  the  anaemia.  Finally  there  may  be  a macrocytic 
anaemia  in  association  with  myxoedema  and  requiring  liver 
therapy  in  addition  to  thyroid  medication. 

The  third  is  nephritis , because  of  the  pallor  and  puffiness, 
but  the  absence,  as  a rule,  of  true  oedema  and  albuminuria 
makes  the  distinction. 

The  fourth  is  neurasthenia — an  old  enemy  to  precision  in 
diagnosis.  One  of  the  worst  cases  of  myxoedema  in  a male 
which  has  come  my  way  was  that  of  a man  in  middle  life 
who,  for  upwards  of  10  years,  had  slowly  been  losing  mental 
and  physical  energy  until  he  was  almost  incapacitated.  He 
had  been  given  the  label  of  neurasthenia.  His  harsh,  dry 


MANIFESTATIONS  OF  THYROID  DEFICIENCY  373 
skin,  his  weary  voice  and  slow  speech,  his  thick  winter 
underclothing  worn  in  midsummer  suggested  the  dia- 
gnosis.  His  case  demonstrates  a real  difficulty  in  diagnosing 
myxoedema,  namely,  its  slow  course  and  insidious  advance. 
Tlixee  of  the  cases  I have  described  gave  histories  of  ten 
years  or  more.  It  is  thus  easier,  sometimes,  for  the  consul- 
tant or  some  one  who  has  never  seen  the  patient  previously 
to  form  his  opinion  than  for  the  family  doctor,  who  must 
endeavour  to  assess  the  meaning  of  subjective  symptoms, 
often  indefinitely  stated  by  the  patient,  and  remains  unim- 
pressed by  physical  or  physiognomical  changes  by  reason 
of  the  very  slowness  of  their  arrival  during  a period,  not  of 
weeks  or  months,  but  years. 

Treatment 

Apart  from  general  hygienic  measures,  treatment  may  be 
condensed  into  the  one  word,  ‘thyroid’.  The  dosage  varies 
with  the  case,  but  large  doses  are  rarely  necessary.  The 
response  to  treatment  becomes  apparent  within  about  three 
weeks.  It  is  well  to  remember  that  most  of  the  proprietary 
preparations  have  their  dosage  expressed  in  terms  of  fresh 
gland,  and  that  gr.  5 of  Tab.  Thyroid  (B.  & IV.),  for  instance, 
is  therefore  equivalent  to  gr.  I of  Thyroid.  Siccum  (B.P.). 
I seldom  find  that  more  than  gr.  3 daily  (or  its  equivalent) 
of  Thyroid.  Siccum  are  necessary  to  control  a fully  developed 
case.  Occasional  adjustments  of  the  dosage  may  be  neces- 
sary, but  the  administration  must  be  continued  for  the  rest 
of  the  patient’s  life.  Iron  or  liver  may  also  be  necessary. 

Some  Other  Manifestations  of  Thyroid  Deficiency 

1.  Minor  hypothyroidism.  For  every  case  of  developed 
myxoedema  which  you  may  see,  and  as  such  it  is  a rare 
disease,  you  will  see  many  cases  of  minor  hypothyroidism. 
In  women  of  a particular  type  it  is  not  uncommon  for  dry- 
ness of  the  skin,  brittleness  of  the  nails,  falling  of  the  hair, 
and  a gain  in  weight  to  accompany  or  follow  the  menopause, 
and  small  doses  of  thyroid  may  here  have  a beneficial  effect. 
Obesity,  without  other  signs  of  hypothyroidism,  is  not 
generally  an  indication  for  thyroid  treatment. 


374  MYXOEDEMA  AND  OTHER 

2.  Creaky  knees.  Some  years  ago  Mr.  E.  G.  Slesinger 
drew  my  attention  to  a type  of  arthritis  affecting  the  knees 
only,  and  occurring  in  women  at  or  after  the  menopause.  I 
have  been  accustomed  to  label  the  condition  ‘creaky  knees’. 
At  times  it  causes  considerable  disability,  with  stiffness, 
weakness,  pain,  and  not  a little  thickening  of  the  joints 
The  patients  ore  particularly  aware  of  their  disability  in 
going  downstairs  or  getting  up  out  of  a low  chair.  They 
generally  show  some  slight  evidences  of  hypothyroidism, 
and  are  often,  but  not  always,  overweight.  Sir.  Slesinger 
told  me  that  they  frequently  improved  in  a striking  way 
under  thyroid  treatment  and  I have  many  times  confirmed 
the  observation.  The  improvement  in  local  symptoms  and 
signs  is  remarkable,  and  this  simple  measure  may  succeed 
when  others  have  been  tried  and  failed.  I do  not  think  the 
effect  can  be  wholly  accounted  for  by  lessened  articular 
stress  through  loss  of  weight. 

8.  Sterility.  I was  once  consulted  by  a married  woman  in 
the  thirties  for  general  unfitness  and  dyspepsia.  She  also 
confessed  that  for  years  she  had  been  hoping  in  vain  for  a 
baby.  She  had  an  exceedingly  dry  skin.  Her  health  im- 
proved under  thyroid  and  she  later  reported  that  her  wish 
had  at  last  been  fulfilled.  On  one  other  occasion  I have 
recorded  pregnancy  following  thyroid  treatment  for  hypo- 
thyroidism. I think  it  not  improbable  that  the  thyroid  was 
responsible,  but  you  must  not  expect  thyroid  to  bring  about 
this  happy  result  unless  there  are  other  indications  of  defec- 
tive thyroid  secretion. 

4.  Chronic  oedema.  A spinster,  aged  GG,  consulted  me  for 
extremely  thickened,  stiff,  and  creaky  knees.  In  addition 
both  her  legs  were  enormously  swollen  with  a true  but  very 
solid  oedema,  so  that  their  appearance  suggested  elephan- 
tiasis. To  this  condition  she  had  become  resigned  as  she  had 
had  it  for  many  years;  in  fact,  she  had  consulted  Guy's 
physicians  of  two  previous  generations  about  it.  Mentally 
she  was  very  active  and  alert,  and  although  very  stout,  she 
did  not  show  other  signs  of  hypothyroidism.  I prescribed 
thyroid  because  of  the  creaky  knees,  and  to  her  great 
pleasure  and  my  surprise,  remarkable  improvement  followed 


MANIFESTATIONS  OF  THYROID  DEFICIENCY  875 
not  only  in  respect  of  the  knees,  but  also  in  respect  of  the 
oedema,  which  gradually  melted  away.  She  lost  3 st.  in 
weight  and  the  circumference  of  her  ankles  was  reduced 
from  13|  to  9|  in.  This  was  one  of  those  happy  and  unex- 
pected results  we  meet  with  from  time  to  time,  but  it  fol- 
lowed upon  a treatment  not  without  a rational  basis. 

In  conclusion  I would  remind  you  of  some  historical  points 
concerning  myxoedema.  It  was  first  described  by  a Guy’s 
physician,  Sir  William  Gull,  who  in  1873  read  a paper  before 
the  Clinical  Society  of  London  ‘ On  a Cretinoid  State  super- 
vening in  Adult  Life  in  Women’.  He  depicted  all  the  essen- 
tial characters  of  the  disease,  and  no  one  has  improved  upon 
his  clinical  portraiture.  The  morbid  anatomy  and  histology 
were  described  four  years  later  by  William  Ord,  who  refers 
to  the  ‘jelly-like  swelling  of  the  connective  tissue,  chiefly,  if 
not  entirely,  consisting  in  an  overgrowth  of  the  mucus-yield- 
ing cement’;  he  also  proposed  the  name  of  myxoedema. 
Hilton  Fagge,  in  a paper  on  * Sporadic  Cretinism  ’ (1871),  had 
already  associated  the  physical  changes  with  atrophy  of  the 
thyroid  gland.  In  1892  Hector  Mackenzie  showed  that 
thyroid  feeding  would  cure  the  disease. 


XXX 


MENINGITIS  AND  MENINGISM1 

Some  of  you  will  remember  having  seen  in  my  wards  during 
the  early  weeks  of  the  present  year  two  cases  of  meningitis  in 
small  children,  the  one  meningococcic  and  the  other  tuber- 
culous, the  first  progressing  satisfactorily  to  recovery'  after 
treatment  with  serum ; the  second,  as  was  inevitable,  ending 
fatally.  Shortly  afterwards  I saw  elsewhere,  in  quick  succes- 
sion, two  further  cases  presenting  the  syndrome  of  meningeal 
irritation,  but  in  neither  case  as  a result  of  meningeal  in- 
fection. This  small  group  of  cases  not  unnaturally  set  me 
thinking  of  the  various  conditions  in  which  I had  encoun- 
tered the  signs  and  symptoms  commonly  considered  as 
peculiar  to  meningitis.  It  occurred  to  me  that  it  might  not 
be  amiss  to  do  some  of  this  thinking  aloud  at  a clinical 
lecture. 

I propose  to  give  you,  first  of  all,  a brief  account  of  these 
four  cases,  together  with  a description  of  four  others  from 
among  my  files;  secondly,  to  consider  how  far  the  case- 
histories  were  in  agreement,  in  what  respects  they  differed, 
and  what  were  the  points  of  differentiation  which  led  to  the 
final  diagnosis  in  each  instance ; and,  thirdly,  to  extract  from 
the  whole  series  a common  group  of  symptoms  with  a view 
to  deciding,  so  far  as  we  may,  their  specific  import. 

By  way  of  introduction,  let  me  remind  you  that  we  gener- 
ally mean  by  the  term  ‘meningitis’  a pathological  state 
involving  inflammation  (generally  an  infective  inflamma- 
tion) of  the  meninges,  and  by  ‘meningism’  a clinical  state 
suggestive  of  meningitis,  but  lacking  such  final  proofs  of 
meningitis  as  an  increase  in  the  cellular  content  of  the 
cerebrospinal  fluid  or  the  presence  of  organisms.  As  I shall 
hope  to  show,  these  terms,  although  sometimes  used  by  the 
physician  in  a differential  sense,  are  not  contradistinctive, 
for  every  case  of  active  meningitis  manifests  meningism 
and  (although  this  might  not  be  so  universally  approved) 

1 Guy's  Ilosp.  Gazelle,  1032,  ilvi.  123. 


MENINGITIS  AND  MENINGISM  377 

every  patient  with  meningism  has,  I believe,  irritation 
of  his  meninges  or  a mild  meningitis,  even  though  this  be 
not  due  to  the  presence  of  bacteria  or  proclaimed  by  the 
visible  products  of  bacterial  inflammation. 

What  are  the  symptoms  and  signs  which  accompany 
meningism  and  meningitis?  Severe  headache  generally, 
photophobia  frequently,  vomiting  not  infrequently  are 
among  the  patient’s  complaints.  The  vomiting  and  head- 
ache are  probably  symptomatic  of  the  increased  intracranial 
pressure  rather  than  of  the  local  inflammation  of  the  mem- 
branes. Neck-rigidity  in  some  degree,  with  head-retraction 
in  extreme  cases,  and  a positive  ICemig’s  sign  are  the  most 
important  physical  signs.  Neck-rigidity  is  best  tested  for  by 
inserting  the  fingers  of  the  two  hands  behind  the  occiput  of 
the  patient  and  gently  attempting  to  raise  the  head  from 
the  pillow  so  as  to  approximate  the  chin  to  the  chest.  Any 
pain  so  caused  will  be  immediately  apparent  in  the  patient’s 
face.  Objectively  there  is  a sensation  of  stubborn  stiffness 
or  involuntary  resistance,  and  the  intended  approximation 
of  chin  to  chest  is  found  to  be  prevented  in  varying  degree. 
To  elicit  Kemig’s  sign  we  flex  the  thigh  to  a right  angle  with 
the  trunk  and  then  gently  straighten  the  leg  on  the  thigh. 
In  a healthy  child  the  leg  will  easily  straighten  completely. 
In  older  subjects  it  wall,  at  any  rate,  extend  sufficiently  to 
form  a wide  obtuse  angle  with  the  thigh.  When  the  sign  is 
positive  a sense  of  fixed  resistance,  sometimes  almost  sug- 
gesting ankylosis,  is  felt  as  the  knee  reaches  or  just  surpasses 
a right  angle.  If  the  pressure  is  continued  pain  is  caused  and 
the  other  leg  is  sometimes  involuntarily  flexed.  Both  with 
neck-rigidity  and  Kernig’s  sign  there  is  some  correspondence 
between  the  activity  of  the  inflammation  and  the  positive- 
ness of  the  sign. 

Now  let  us  turn  to  our  cases. 

Case  1.  A male  baby,  aged  9 months,  was  admitted  to  Maty 
Ward  on  26  December  1931  with  high  fever,  up  to  106°,  and  rapid 
respirations.  We  were  anticipating  pneumonia,  but  no  localizing 
signs  appeared  until  the  fifth  day,  when  convulsive  twitchings  of  the 
right  side  and  transient  strabismus  were  noticed  and  a slight  degree 
of  neck-rigidity  and  Kemig's  sign  were  demonstrated.  A faintly 
turbid  cerebrospinal  fluid  under  increased  pressure  was  withdrawn 


878  MENINGITIS  AND  MENING1SM 

by  Mr.  G.  V.  Steward,  and  the  laboratory  reported  a polymorpho- 
nuclear increase  and  meningococci.  Anti-mcningococcal  scrum  was 
given  on  six  occasions  intrathccally  and  the  child  made  a good 
recovery,  complicated  only  by  acute  iritis  with  haemorrhage  into  the 
anterior  chamber  of  the  left  eye.  The  history  and  course  of  this  case 
suggest  a meningococcic  septicaemia  with  a delayed  meningeal  loca- 
lization producing  only  moderate  symptoms.  In  the  majority  of 
cases  of  acute  meningitis  (whether  meningococcic,  pncumococcic,  or 
streptococcic)  the  physical  signs  are  more  pronounced  than  they 
were  in  this  case. 

Case  2.  A boy,  aged  0,  was  admitted  to  Addison  Ward  on  14 
January’  1D32  for  fever  and  profound  lethargy.  His  earlier  life  had 
been  healthy  excepting  for  winter  cough.  At  the  end  of  November 
1031  he  sustained  a slight  concussion.  He  was  then  well  until  Christ- 
mas, when  he  had  pleuritic  pain  in  the  left  chest.  On  Christmas  Day 
he  was  quite  happy,  but  on  27  December  he  was  quiet  and  feverish, 
and  thereafter  remained  subdued  until  11  January,  when  he  began 
to  complain  of  occipital  headache.  On  1 3 January*  a lumbar  puncture 
was  performed  by  Dr.  W.  F.  Hudson,  of  Banbury*.  On  admission,  he 
lay  flat  on  his  hack  with  his  eyes  half-closed.  Ncck-rigidity  and  Ker- 
nig’s  sign  were  present,  but  in  very  slight  degree.  The  abdomen  was 
retracted.  He  resented  examination,  and  when  bis  night-shirt  was 
raised  to  allow  examination  of  the  abdomen  he  tried  to  pull  it  down 
again  with  an  irritable  protest  and  grimace,  exhibiting  what  has  been 
described  as  ‘Stocker’s  sign’.  James  Stocker,  who  was  apothecary  to 
Guy’s  Hospital  for  many  years  until  shortly  before  his  death  in  1878, 
pointed  out  that  this  type  of  irritability  distinguished  cerebral  cases 
from  cases  of  illness  with  apathy  due  to  the  then  prevalent  ‘fever’. 
The  cerebrospinal  fluid  was  under  pressure  and  clear,  and  an  excess 
of  lymphocytes  with  tubercle  bacilli  was  reported.  The  boy  become 
coma t os b with  high  pyrexia,  and  died  on  21  January  1032. 

The  mode  of  onset  was  very  different  in  these  two  cases, 
acute  with  high  fever  in  the  first,  insidious  with  increasing 
stupor  in  the  second.  The  neck-rigidity*  and  Kemig’s  sign 
were  not  pronounced  in  either,  but  less  so  with  the  less  ful- 
minating infection.  The  decubitus  and  Stocker’s  sign  were 
most  characteristic  in  the  boy  with  tuberculosis,  and  the 
earlier  history  of  a pleurisy*  gave  evidence  of  the  primary* 
lung  focus,  later  revealed  at  the  post-mortem  examination. 

Cask  8.  In  January  1032 1 saw,  with  Dt.G.E.W.  Lacey,  a nervous 
and  childless  married  woman,  aged  42,  who  gave  the  following  story. 
She  Iiad  always  been  liable  to  headaches  and  fainting.  In  the  previous 
week  she  had  been  busy  looking  after  neighbours  with  influenza. 
Three  days  before  the  consultation,  while  at  stool,  she  was  suddenly* 


MENINGITIS  AND  MENINGISM  379 

seized  with  intense  pain  in  the  head.  She  managed  to  get  to  her  bed 
and  there  lay,  apparently  unconscious,  for  2£  hours,  and  2 hours  later 
she  was  still  stuporose.  The  knee-jerks  were  exaggerated,  and  Dx. 
Lacey  queried  a left  extensor  plantar  response.  The  temperature  on 
the  first  day  was  99.  When  I saw  her  she  was  rational  and  afebrile, 
but  still  complaining  of  headache.  There  was  a slight  but  definite 
neck-rigidity  with  a positive  Kernig's  sign.  The  left  plantar  response 
was  definitely  extensor.  Her  blood-pressure  was  200-130.  She  recol- 
lected that  3 months  previously,  when  scrubbing  a floor,  she  had  been 
seized  with  a similar  headache,  which  lasted  some  hours.  I diagnosed 
‘sub-arachnoid  haemorrhage’,  and,  as  she  was  so  clearly  improving, 
decided  against  a lumbar  puncture.  The  absence  of  pyrexia  after  the 
first  day  and  of  serious  constitutional  disturbance  opposed  any  acute 
form  of  meningitis,  and  the  high  blood-pressure  suggested  the  more 
probable  pathology. 

Case  4.  A prosperous  business  man  of  plethoric  type,  who  was 
known  to  have  a high  blood-pressure,  was  noticed  one  evening  to  be  a 
little  peculiar  in  his  behaviour.  The  next  morning  he  vomited  three 
times  in  quick  succession  and  was  dazed.  He  was  put  to  bed  and 
remained  there  in  a semi-stuporose  condition  for  the  next  ten  days. 
When  I saw  liim,  in  consultation  with  Dr.  W.  J.  Montague,  he  was 
lying  with  his  hand  pressed  to  Ids  forehead,  but  did  not  admit  to 
much  pain.  He  was  restive  at  night  and  required  catheterization. 
His  temperature  fluctuated  between  09  and  101.  There  was  distinct 
neck-rigidity  with  a positive  Kernig’s  sign.  We  also  noticed  a slight 
weakness  of  the  right  arm  and  leg  as  compared  with  the  left,  and  the 
finger-nose  test  was  performed  badly  with  the  right  hand.  A lumbar 
puncture  performed  by  Dr.  Montague  before  my  arrival  showed  an 
intimately  blood-stained  fluid,  the  blood  being  largely  laked.  The 
blood-pressure  was  100-110.  Here  the  diagnosis  of  hyperpiesia  with 
sub-arachnoid  haemorrhage  was  confirmed  by  the  lumbar  puncture. 

Sub-nrachnoid  haemorrhage  occurring  spontaneously  in  a 
patient  with  high  blood-pressure  is  less  likely  to  give  rise  to 
difficulties  than  the  same  accident  in  a child  or  young  adult. 
Here,  as  Sir  Charles  Symonds1  and  others  have  shown, 
the  haemorrhage  usually  comes  from  a small  aneurysm, 
either  congenital  or,  in  cases  with  infective  endocarditis, 
resulting  from  embolism. 

Case  5.  In  1929  I saw  at  the  Blackheath  and  Charlton  Hospital, 
with  Dr.  It.  W.  Warrick,  a boy,  aged  14,  who  had  been  found  uncon- 
scious in  the  lavatory  4 days  previously.  On  admission,  neck-rigidity 
was  discovered  and  a lumbar  puncture  had  been  performed,  giving  a 

1 Guy's  Hospital  Heports,  1923,  Ixxiii.  139. 


380  MENINGITIS  AND  MENING1SM 

blood-stained  fluid  with  no  organisms.  On  recovering  consciousness, 
lie  was  found  to  liavc  a right  hemiplegia.  Slight  pyrexia  continued 
for  the  next  3 days.  Neck-stiffness  and  Kernig’s  sign  were  well 
marked  at  the  time  of  my  visit.  I noticed  weakness  with  increased 
reflexes  of  the  right  nnn  and  leg  and  n right  extensor  plantar  response. 
The  cerebrospinal  fluid  that  day  was  pale  yellow  and  showed  an 
increase  of  protein.  The  hoy’s  previous  good  health,  the  abrupt  onset 
and  localizing  signs,  and  the  changes  in  the  cerebrospinal  fluid  made 
a leaking  congenital  aneurysm  an  almost  certain  diagnosis.  IVithin 
a few  days  of  the  accident  he  was  cheerful  and  able  to  take  food  in  a 
way  which  would  have  been  most  unusual  in  a child  with  meningitis. 

Here,  then,  we  have  three  cases  of  haemorrhage  on  the  sur- 
face of  the  brain  causing  the  same  leading  symptoms  which 
we  have  just  considered  in  cases  of  infective  meningitis. 
With  a widely  differing  pathology  we  find  headache,  fever, 
neck-rigidity,  and  Kcmig’s  sign  common  to  these  conditions. 
I may  remind  you  that  haemorrhage  into  other  serous 
cavities,  such  as  the  peritoneum  or  a joint,  may  also  closely 
simulate  inflammation  of  their  membranes.  You  will  observe 
that  in  each  of  the  cases  of  meningeal  haemorrhage  some 
additional  feature,  such  as  abrupt  onset  (in  two  cases  in  the 
lavatory),  high  blood-pressure,  or  some  indication  of  local 
cerebral  damage  was  present  to  help  in  the  differentiation 
from  infective  meningitis. 

Case  C.  In  May  1028  I saw  on  the  tenth  day  of  his  illness,  with 
Dr.  J.  IV'.  Ensor,  a boy  of  17  years  who  had  complained  primarily  of 
headache,  which  later  became  severe  and  was  associated  with  pain 
and  stiffness  in  the  limbs.  On  the  fifth  day  he  tried  to  get  out  of  bed 
and  found  that  his  legs  would  not  support  him.  Ills  temperature, 
which  never  rose  above  101,  was  normal  on  the  seventh  day.  The 
headache  had  departed,  but  I still  found  well-marked  neck-stiffness 
and  Kernig’s  sign.  In  addition,  however,  he  had  a flaccid  weakness  of 
both  quadriceps  with  absent  knee-jerks  and  left  ankle-jerk  and  absent 
abdominal  reflexes.  The  case  was  one  of  anterior  poliomyelitis. 

The  cerebrospinal  fluid  in  acute  poliomyelitis  frequently 
shows  a lymphocytic  increase.  We  have  here  another 
example  (although  the  main  incidence  of  the  disease  is  on 
other  parts)  of  infection  of  quite  another  type  which  some- 
times affects  the  meninges. 

Case  7.  A young  nurse  was  admitted  to  Maiy  Ward  with  general 
superficial  adenitis  due  to  an  accidental  infection  with  syphilis.  After 
her  first  dose  of  NA.B.  she  developed  acute  cerebral  and  meningeal 


MENINGITIS  AND  MENINGISM  381 

symptoms,  including  severe  headache,  neck-stiffness,  convulsions, 
and  a slow  pulse.  The  cerebrospinal  fluid  showed  an  excess  of  lym- 
phocytes. Later  she  developed  a right-sided  hemiplegia.  After  a long 
illness  and  intensive  treatment  with  mercury,  iodides,  and  bismuth, 
all  signs  eventually  cleared  up.  The  Wassermann  reaction  of  blood 
and  fluid  became  negative,  the  cell-count  became  normal,  and  she  was 
able  to  return  to  her  work  and  has  since  kept  well. 

This  is  not  a common  story.  I mention  it  merely  as  an 
example  of  one  other  type  of  infection  which  may  give  rise 
to  meningitic  manifestations  when  abruptly  activated. 

Case  8 . Lastly  we  come  to  a case  of  what  would  be  styled  ‘ mening- 
ism*  in  the  more  accepted  sense  of  the  term.  A year  ago  a small 
boy  was  admitted  to  one  of  my  cots  in  Mary  Ward.  In  the  surgery 
his  symptoms  were  mainly  abdominal,  and  appendicitis  had  been 
suspected.  Shortly  after  admission  he  developed  neck-rigidity  and 
Kernig’s  sign.  He  may  be  said  to  have  shown  ‘ peritonism  ’ and 
‘meningism’  in  quick  succession.  He  then  developed  signs  of  an 
apical  pneumonia  and,  later,  an  empyema,  and  finally  acquired  scarlet 
fever  and  died  in  the  isolation  room.  A lumbar  puncture  performed 
during  the  stage  of  meningism  showed  that  the  fluid  was  under 
definitely  increased  pressure  but  there  were  no  cellular  abnormalities. 

Meningism  of  this  type  is  a not  infrequent  occurrence  in 
children  with  pneumonia  or  otitis  media.  That  the  nervous 
system  in  childhood  is  a more  sensitive  machine  is  shown  by 
the  frequency  of  convulsions  in  the  tender  years.  Although 
I was  frequently  compelled  to  perform  a lumbar  puncture  in 
eases  of  typhoid  fever  and  trench  fever  during  the  1014-18 
War  on  account  of  intense  headache  and  a pseudo-Kernig’s 
sign  due  to  muscular  pain  and  stiffness,  I cannot  recollect 
that  I have  ever  seen  pronounced  meningism  apart  from 
meningitis  or  meningeal  haemorrhage  in  an  adult.1 

Now  if  we  are  to  accept,  as  seems  reasonable,  that  the 
meningism  (i.e.  Kernig’s  sign  and  neck-rigidity)  in  cases 
1 to  7 was  expressive  of  a genuine  meningeal  inflammation, 
it  becomes  difficult  to  believe  that  the  indistinguishable 
meningism  of  pneumonia  and  otitis  media  in  children  can 

1 Since  this  lecture  was  given  we  have  had  a case  in  Clinical  Ward  of  a 
man  with  an  epidural  abscess  who  showed  meningism.  His  cerebrospinal 
fluid  was  under  increased  pressure,  but  quite  clear.  It  showed  no  organisms, 
but  an  increase  both  of  polymorphonuclear  ceils  and  of  lymphocytes.  He 
had,  therefore,  a mild  meningitis  due  to  a neighbouring  infection.  Later 
he  succumbed  to  a septic  meningitis. 


382  MENINGITIS  AND  MENINGISM 

have  an  alternative  explanation.  And  yet  it  is,  I fancy,  quite 
commonly  supposed  that  meningism  of  this  type  is  due  to 
some  vague  ‘reflex  irritability’,  or  else  the  syndrome  is  left 
unexplained.  Is  it  not  too  readily  assumed  that  an  absence 
of  cells  and  organisms  or  a negative  inspection  after  death 
establishes  the  absence  of  meningitis  ? I would  rather  argue 
that  meningism  is  a specific  reaction  more  delicate  in  its  pro- 
clamations than  the  pathologist’s  microscope,  and  that  there 
is  a genuine  irritation,  or  non-infective  inflammation,  of  the 
meninges  in  these  pneumonic  and  otitic  cases  due,  probably, 
to  the  chemical  products  of  fever  or  contiguous  infection. 
We  have  further  observations  in  support  of  this.  In  one  case 
described  (Case  8),  although  there  was  no  cellular  increase 
the  pressure  of  the  cerebrospinal  fluid  was  conspicuously 
raised.  If  the  pressure  of  the  fluid  is  raised,  there  must  either 
be  some  process  stimulating  an  increased  secretion  or  some 
interference  with  absorption.  In  other  serous  cavities  of 
the  body,  such  as  the  knee-joint,  we  know  that  effusion 
may  occur  without  the  presence  of  bacteria  or  leucocytes. 
Furthermore,  I can  relate  another  case  of  meningism  with 
pneumonia  in  a child  in  which,  with  a clear  fluid,  we  yet 
discovered  a few  polymorphonuclear  cells  in  the  centrifu- 
galized  deposit,  and  an  adult  case  of  presumed  meningitis 
in  a soldier  in  which  one  colony  of  meningococci  grew  from 
a clear  fluid  and  the  patient  proceeded  to  get  well  after  a 
single  puncture.  Findings  such  as  these  seem  to  me  to 
establish  the  link  between  the  cases  of  supposedly  non- 
meningitic  meningism  and  the  cases  with  accepted  proofs 
of  meningitis.  With  the  help  of  such  observations  may  we 
not  argue  that  meningism  (that  is  to  say,  the  syndrome  in- 
cluding neck-rigidity  and  Kcmig’s  sign)  is  always  specific 
of  meningitis,  even  if  that  meningitis,  as  in  the  case  of 
sub-arachnoid  haemorrhage  and  the  pneumonic  and  otitic 
forms,  is  aw  aseptic,  meningitis  and  unassociated  with  gross 
products  of  inflammation  in  the  cerebrospinal  fluid  ? 

While  they  are  specific  of  meningeal  irritation,  the  symp- 
toms of  meningism  are  not,  however,  specific  of  any  type  or 
cause  of  irrita  tion.  This  is  true  of  all  well-defined  symptoms. 
They  constantly  specify  a type  or  mode  of  physiological 


MENINGITIS  AND  MENINGISM  883 

disturbance,  but  they  do  not  in  themselves  indicate  the 
particular  cause  of  the  disturbance.  For  a full  diagnosis 
other  clues  must  be  sought  in  the  age  and  the  general 
condition  of  the  patient,  in  the  history,  and  in  associated 
symptoms  and  signs. 

In  conclusion,  there  are  four  main  groups  of  cases  in  which 
meningism  may  be  observed: 

1.  Acute  pyogenic  meningitis  (meningococcic,  pneumo- 
coccic,  streptococcic). 

2.  Sub-acute  meningitis  complicating  general  tubercu- 
losis, poliomyelitis,  or  activated  syphilis. 

3.  The  aseptic  meningitis  of  sub-arachnoid  haemorrhage. 

4.  The  meningeal  irritation  or  aseptic  meningitis  of 
pneumonia  and  otitis  media  in  children. 

With  ordinary  clinical  care  it  should  be  possible  to  place 
a case  in  one  of  these  four  groups,  and  often  enough  to  give 
a correct  opinion.  With  the  aid  of  the  lumbar  puncture 
needle  an  accurate  diagnosis  can  generally  be  established. 


XXXI 

SOME  ALARMING  SEIZURES1 

In  the  course  of  medical  practice  we  are  confronted  from 
time  to  time  by  peculiar  'seizures'  or  ‘nerve  storms', 
which  lack  conformity  with  the  more  familiar  descriptions. 
Some  of  these  seizures  cause  great  alarm  to  their  victims, 
in  that  they  seem  to  threaten  paralysis,  spcechlessness, 
unconsciousness,  or  even  death  itself,  or  because  they  occa- 
sion states  of  profound  instability  and  prostration.  The 
appearance  and  sufferings  of  the  patients  during  these 
attacks  may  further  alarm  relatives  or  onlookers,  and  even 
the  medical  man,  unless  he  be  familiar  with  the  true  nature 
of  the 4 seizures  ’ or  fully  alive  to  the  history  of  the  case,  may 
be  taken  unawares,  and  feel  so  dubious  about  their  purport 
and  outcome  as  to  be  unable  to  give  a reassuring  prognosis. 

And  yet  the  seizures  which  I have  in  mind  are  all  consis- 
tent with  long  life  and  with  good  health  at  other  times. 
Those  with  the  more  local  effects  may  simulate  or  suggest 
organic  disease  of  the  brain;  those  causing  serious  insta- 
bility may  also  be  wrongly  attributed  to  cerebral  vascular 
disease  or  cerebral  tumour;  those  which  cause  pallor, 
distress,  disturbances  of  pu/se-rate,  praecordial  pain  or  dis- 
comfort and,  more  rarely,  loss  of  consciousness,  are  apt  to 
be  ascribed  to  disease  of  the  heart.  We  might  reasonably 
include  in  this  category  ordinary  faints  or  syncope  and 
epileptic  attacks,  and  Gowers  [1],  who  did  more  to  illumine 
this  subject  than  any  one  else,  discussed  together  under 
the  broad  heading  of  The  Borderland  of  Epilepsy,  syncope, 
vertigo,  and  certain  other  ‘nerve  storms’  to  be  described. 

Fainting  and  epilepsy,  as  being  better  knowm,  I shall  not 
consider  here.  The  particular  seizures  which  I wish  to 
review  include  the  aphasic,  hemiplegic,  and  vertiginous 
varieties  of  migraine ; vertigo  whether  due  to  labyrinthine 
disease  or  more  transient  vestibular  disturbance ; and  the  so- 
called  vasovagal  attacks  of  Gowers.  If  we  except  Iabyrin- 

1 British  Med.  Joum.,  1034, 1.  89. 


SOME  ALARBUNG  SEIZURES  385 

thine  vertigo  there  is  no  demonstrable  organic  basis  for  any 
of  these  seizures.  The  physical  overhaul  between  attacks, 
unless  there  be  a coincidental  pathology,  gives  a negative 
result.  They  are  therefore  placed  in  the  category  of  the 
* paroxysmal  neuroses  *.  In  the  migrainous  episodes  tempera- 
ment and  heredity,  sometimes  with  idiosyncrasy  or  allergy 
on  the  one  hand,  and  transient  disturbances  of  physiological 
equilibrium  due  to  fatigue,  worry,  eyestrain,  constipation, 
or  mental  stress  on  the  other,  may  all  play  a determining 
part.  To  no  inconsiderable  extent  the  same  influences  play 
a part  in  increasing  the  liability  to  vertigo  and  vasovagal 
attacks.  Anxiety  of  mind  occasioned  by  the  symptoms 
themselves,  and  the  subsequent  prostration  when  the  storm 
is  past,  are  apt  to  keep  the  patient  in  on  unduly  receptive 
state,  and  so  prone  to  further  storms. 

It  is  my  purpose  to  amplify  a brief  general  account  of 
these  interesting,  and  by  no  means  rare,  neuroses  with  some 
case-histories  illustrating  their  symptomatology,  and  justi- 
fying, as  I think  you  will  agree,  their  inclusion  in  the  list 
of  the  ‘alarming  seizures’.  Thereafter  I shall  shortly  con- 
sider a few  important  principles  in  the  management  of  cases. 

Migraine  and  its  Variants 

If  we  are  to  study  its  less-frequent  variants  we  should 
start  with  a clear  image  of  the  better-known  phenomena  of 
migraine.  As  commonly  seen  it  is  a disorder  chiefly  of  the 
active  period  of  adult  life,  affecting  both  sexes,  depending 
strongly  upon  hereditary  endowment,  and  showing  a ten- 
dency, better  marked  in  men  than  in  women,  to  sponta- 
neous remission  after  the  age  of  50.  It  is  characterized  by 
symptoms  of  very  variable  severity,  and  occurs  in  intermit- 
tent paroxysms  separated  by  days,  weeks,  or  months.  The 
paroxysms  come  ‘out  of  the  blue  and  often  for  no  apparent 
reason ; on  the  previous  day  the  patient  may  have  felt  parti- 
cularly well.  They  commonly  start  on  waking  in  the  morn- 
ing. The  first  symptom  may  be  a hemicranial  brow  ache, 
or  more  generalized  headache,  but  before  this  there  is  often 
a passing  disturbance  of  vision.  Fortification  spectrum  or 
teichopsia  on  the  one  hand,  or  a blind  patch  or  hemianopia 


3SG 


SOME  ALARMING  SEIZURES 
on  the  other,  are  the  commoner  forms  of  aura.  The  head- 
ache in  a case  of  average  severity  becomes  more  intense 
during  the  day ; sometimes  it  is  completely  crippling,  and 
necessitates  retirement  to  a quiet  and  darkened  room. 
Nausea  or  repeated  retching  and  bilious  vomiting  follow. 
The  patient  looks  pale  and  ill,  with  dark  rings  under  the 
eyes.  Twelve  hours  is  a usual  duration  for  the  attack, 
but  it  may  be  prolonged  to  twenty-four  hours  or,  more 
rarely,  through  two  or  three  days.  There  remains  a sense 
of  prostration,  which  takes  another  day  or  two  to  pass. 
Cold,  fatigue,  worry,  eyestrain,  train  and  motor  journeys, 
and  certain  foodstuffs  or  beverages — notably  rich  or  fried 
foods,  chocolate,  and  eggs — are  among  the  recognized 
precipitating  causes.  Mental  workers  who  get  little  exercise 
are  more  prone  to  the  disorder  than  others.  The  menstrual 
period  and  the  menopause  in  women  are  particular  times 
of  aggravation. 

Some  patients  escape  with  occasional  attacks  of  hemi- 
anopia  or  teichopsia;  some  with  slight  headaches  which 
cause  little  or  no  interruption  to  work;  some  experience  the 
more  familiar  attacks  at  one  time,  and  at  another  the  apha- 
sic,  hemiplegic,  or  vertiginous  variants  which  I am  about 
to  describe.  There  are  also  variants  of  another  kind,  in 
which  abdominal  symptoms  predominate,  whether  as  sick- 
ness, diarrhoea,  or  pain,  or  some  combination  of  these  with 
a general  malaise,  but  always  tending  to  a periodic  or  inter- 
mittent behaviour,  and  an  equivalent  duration  of  symptoms. 
Sometimes  the  abdominal  manifestations  are  severe  enough 
to  suggest  food  poisoning  or  an  abdominal  emergency.  In 
some  cases  there  is  a vague  sense  of  soreness  or  discomfort 
about  the  liver  region,  and  a look  of  sallowness  almost 
approximating  to  icterus.  Gall-bladders  have  been  removed 
in  cases  of  migraine  misdiagnosed  as  cholecystitis.  If  a 
barium-meal  examination  is  made  during  an  attack  of 
migraine  or  migrainous  dyspepsia  the  stomach  is  found  to 
be  inert ; it  may  take  upwards  of  six  hours  to  empty,  and  I 
have  seen  one  case  diagnosed  as  pyloric  stenosis  on  this 
account. 

In  aphasic  and  hemiplegic  migraine,  usually  on  a basis  of 


SOME  ALARMING  SEIZURES  887 

the  more  typical  ocular  and  hemicranial  symptoms,  there 
is  superimposed  a confusion  of  speech,  the  patient  knowing 
well  what  he  wants  to  say,  but  being  unable  to  say  it.  With 
this  there  may  be  a sense  of  weakness  in  the  arm,  or  sensa- 
tions of  numbness  or  tingling  in  the  hand  and  lips  and 
face  of  one  side.  More  rarely  there  is  motor  weakness  or 
even  a transient  paralysis.  It  can  well  be  understood  how 
‘strokes’  are  feared,  or  cerebral  thromboses  actually  dia- 
gnosed in  such  cases.  The  symptoms,  however,  pass  over 
quickly  with  the  rest  of  the  storm,  and  leave  no  relics 
behind  them.  Moreover,  they  can  occur  in  subjects  in 
whom  it  would  be  unreasonable,  on  the  score  of  age,  history, 
and  physical  findings,  to  suspect  vascular  disease,  and  there 
is  often  a personal  or  family  history  of  indisputable  migraine. 

Vestibular  or  vertiginous  migraine  is  characterized  by 
attacks  of  profound  giddiness,  instability,  collapse,  and 
vomiting,  indistinguishable  in  the  main  features  of  the 
attack  from  M&ii&re’s  syndrome,  but  separable  (though 
often  with  difficulty)  from  the  recurrent  vertigo  of  laby- 
rinthine disease  by  a history  of  previous  migraine  or  asso- 
ciated migrainous  phenomena,  and  by  the  absence  of  any 
evidence  of  aural  disease  such  as  deafness  or  tinnitus. 

Aphasic  and  Hemiplegic  Migraine 

Case  1.  A young  married  woman,  aged  31 , of  sensitive,  intelligent 
type,  was  brought  to  me  for  attacks  characterized  by  partial  loss  of 
vision,  headache,  numbness  in  the  lips  and  one  or  other  arm,  and  loss 
of  speech.  The  headache  was  localized  over  one  brow,  and  preceded 
the  aphasia.  During  the  attack  she  knew  exactly  what  she  wanted 
to  say,  but  could  not  say  it,  and  was  aware  that  she  was  ‘talking 
rubbish’.  The  attacks  ended  with  vomiting,  griping  epigastric  pain, 
and  diarrhoea.  They  lasted  for  4 to  C hours,  and  were  followed  by 
prostration  enduring  for  2 or  8 days.  They  had  caused  her  and  her 
relatives  the  greatest  alarm  and  anxiety.  On  one  occasion  when  the 
left  arm  was  numb  she  had  no  aphasia;  there  was  well-marked 
aphasia  on  each  occasion  when  the  right  arm  was  numb.  She  had 
other  attacks  of  an  abdominal  type,  which  had  at  first  been  ascribed 
to  ‘food  poisoning’,  and  others  with  headache  and  giddiness.  Con- 
stipation and  nervous  strain  were  particular  determining  factors. 

Case  2.  A small,  healthy-looking  girl,  aged  12,  experienced  6 
attacks  in  the  course  of  8 months,  in  which  she  complained  of  a feeling 


888  SOME  ALARMING  SEIZURES 

of  numbness  and  weakness  ‘all  down  one  side’.  Although  she  could 
move  the  arm  she  was  quite  unable  to  hold  a cup.  These  symptoms 
would  endure  for  about  10  minutes,  and  were  followed  by  visual  dis- 
turbance and  a headache,  which  persisted  throughout  the  day.  In 
one  attack  she  vomited.  In  all  of  them  she  ‘went  off  her  food',  be- 
came drowsy,  and  for  the  next  day  or  two  was  lacking  in  energy;  her 
breath  and  tongue  were  unpleasant.  Her  mother  had  had  ‘terrible* 
periodic  headaches  throughout  her  life,  and  at  odd  intervals  liad  ex- 
perienced similar  feelings  in  the  arm,  and  on  one  occasion  had  dropped 
a teapot.  A younger  brother  of  the  patient  had  ‘acidosis’  attacks. 

The  hemiplegic  symptoms  are  usually,  as  in  the  first  case, 
of  a sensory  kind,  and  referred  to  as  weakness,  numbness, 
or  tingling,  rather  than  as  loss  of  power,  but  actual  loss  of 
power  may  occur  as  in  the  second  case.  Although  slight 
paraesthesiae  and  transient  dizziness  were  mentioned  in 
other  cases,  X have  encountered  only  six  examples  of  aphasic 
and  hemiplegic  migraine,  and  the  same  number  of  vertigi- 
nous seizures  among  213  migrainous  patients.  Probably 
the  neurologists  see  a higher  proportion  of  these  interesting 
cases. 


Vestibular  Migraine 

Case  3.  A man,  aged  48,  whose  mother  had  suffered  from  bilious 
attacks,  complained  that  since  boyhood  he  bad  been  liable  to  bilious 
attacks  followed  by  extreme  drowsiness.  He  was  even  at  times  found 
asleep  by  the  roadside  on  the  way  home  from  his  work.  (Drowsi- 
ness is  well  recognized  as  an  occasional  manifestation  of  migraine.) 
Latterly  these  attacks  had  taken  on  a new  form,  and  were  character- 
ized by  severe  vertigo  with  sickness,  giving  place  to  the  old  drowsi- 
ness with  slight  headache.  These  attacks  would  come  on  at  any  time, 
but  especially  in  the  morning.  After  them  he  felt  completely  ‘washed 
out’.  Cigars,  a missed  bowel  movement,  worry,  and  a stuffy  room 
were  recognized  as  determining  causes.  There  was  no  evidence  of  ear 
disease. 

Case  4.  A woman,  aged  48,  always  ‘highly  strung’,  had  been  liable 
to  sick  headache  at  long  intervals.  In  some  of  the  attacks  she  was 
temporarily  blind  in  one  eye.  Three  months  before  seeing  me  she  was 
overcome  with  giddiness  one  morning,  ‘everything  went  black’,  and 
she  saw  quivering  specks  of  light.  There  was  much  nausea,  and  she 
did  not  feel  really  well  for  several  days.  A fortnight  later  she  had  a 
similar  seizure,  with  a sensation  of  falling  forward.  Others  followed, 
and  were  accompanied  by  severe  headache,  which  left  her  scalp  sore. 
Aggravating  factors  at  this  period  of  exacerbation  included  great 
domestic  sorrows  and  anxieties,  and  a secondary  anaemia. 


SOME  ALARMING  SEIZURES  889 

We  find,  therefore,  that  the  victims  of  what  we  may  call 
‘ordinary  migraine’  may  at  times  experience  other  types 
of  seizure,  characterized  by  aphasia,  unilateral  sensory  or 
motor  disturbances  in  the  periphery,  and  vertigo.  A careful 
unravelling  of  the  history  and  an  analysis  of  the  symptoms 
in  the  particular  attacks  which  have  caused  alarm  will, 
however,  nearly  always  reveal  their  true  nature.  A family 
history  of  migraine  may  provide  the  necessary  clue.  The 
vertiginous  attacks  clearly  suggest  Mdni&re’s  disease  if  in- 
sufficiently analysed.  We  may  therefore  conveniently  pass 
here  to  a consideration  of  some  other  cases  of  vertigo  of 
varied  aetiology. 


Vertigo 

If  we  exclude  intracranial  disease  and  occasional  causes 
such  as  wax  or  water  in  the  ear,  the  pathologies  underlying 
recurrent  vertigo  include:  (a)  the  otosclerosis  which  occurs 
at  or  after  middle-life,  and  accounts  for  the  majority  of 
cases;  (6)  chronic  otitis  media;  (c)  sudden  accidents  to  the 
labyrinth — inflammatory  or  perhaps  due  to  local  haemor- 
rhage; (d)  vasomotor  disturbances  giving  rise  to  abrupt 
fluctuations  in  the  blood-pressure,  in  which  group  we  may 
probably  include  the  cases  seeming  to  follow  directly  upon 
emotional  stress ; (e)  tobacco  excess ; and  (/)  migraine. 

The  usual  story  of  a major  attack  of  vertigo  is  that  of  a 
middle-aged  subject  who  has  previously  noticed  a slight 
progressive  deafness  and  frequent  tinnitus  in  one  ear,  and  is 
seized,  at  any  time  or  place,  whether  in  the  street  or  in  his 
bed,  with  violent  giddiness,  in  which  objects  seem  to  revolve 
around  him  or  the  floor  appears  to  rise  to  meet  him.  He  is 
compelled  to  hold  on  to  the  nearest  railings  or  to  lie  down, 
but  this  brings  no  relief  to  the  sensations,  which  may  con- 
tinue for  minutes  or  hours.  Repeated  vomiting  may  follow, 
and  sometimes  uncontrollable  diarrhoea.  There  is  great 
prostration  and,  more  rarely,  a feeling  of  impending  dissolu- 
tion as  real  as  that  which  is  recorded  by  sufferers  from  vaso- 
vagal attacks  or  occasionally  in  association  with  the  angina 
pectoris  of  coronary  disease.  As  in  migraine,  pallor,  grey- 
ness, and  coldness  are  noted  by  eyewitnesses.  There  are 


300  S03EE  ALARMING  SEIZURES 

usually  intervals  of  days,  weeks,  or  months  between  the 
major  attacks.  The  patient  is  left  shaken  by  them,  lacking 
in  confidence,  depressed,  unwilling  to  go  out  of  doors,  and 
not  infrequently  with  a persisting  sense  of  slight  unsteadi- 
ness, which  is  worse  in  traffic  or  with  sudden  movements 
of  the  eyes  or  changes  of  posture.  Wien  deafness  in  the 
affected  car  becomes  complete  the  vertiginous  seizures  may 
become  less  frequent  and  sometimes  depart  never  to  return. 

It  is  clear  that  the  labyrinthine  disease,  although  an 
essential  conditioning  factor,  is  not  alone  responsible  for  the 
attacks,  for  if  this  were  so  the  vertigo  would  be  continuous 
instead  of  transient  and  occasional.  Of  the  causes  predispos- 
ing to  the  attacks,  states  of  general  physical  or  psycholo- 
gical unfitness,  such  as  result  from  the  menopause,  or  from 
a too  precipitate  loss  or  gain  in  weight,  fatigue,  anaemia, 
and  mental  anxiety,  are  all  noteworthy.  The  determining 
cause  of  the  individual  seizure  is  hard  to  trace,  but  an  empty 
stomach,  a sudden  movement,  or  a strong  emotion  arc 
among  their  number.  Of  perpetuating  causes  I believe  the 
anxiety  and  apprehension  engendered  by  the  attacks  them- 
selves to  be  real  and  outstanding.  After  nil,  nothing  could 
be  better  devised  to  provoke  a nervous  instability  than 
attacks  of  genuine  physical  instability  coming  on  without 
warning  and  beyond  all  voluntary  control.  A conditioning 
physical  cause  is  also  much  more  likely  to  be  operative 
during  states  of  nervous  tension  and  unrest. 

Case  5.  A woman,  aged  GO,  who  had  previously  consulted  me  for 
other  troubles  of  a minor  kind,  was  seized,  after  a period  of  grave 
family  worry,  with  a succession  of  vertiginous  seizures,  in  which  she 
was  prostrate,  vomited  repeatedly,  and  experienced  much  singing  in 
the  ears,  especially  in  the  left  ear.  She  did  not  sleep,  she  was  terrified 
by  the  attacks,  and  apparently  had  feared  a stroke.  She  had  lost  a 
Stone  in  weight  since  her  previous  visit  to  me  a year  before.  The  only 
physical  finding  was  deafness  in  the  left  ear.  The  entry  in  my  notes 
was  ‘labyrinthine  vertigo ; aggravation  by  fatigue,  loss  of  weight, 
constipation,  and  worry*. 

Case  6.  A man,  aged  54,  stated  that  he  was  well  until  3 years  pre- 
viously, when  something  suddenly  ‘popped’  in  his  left  ear,  and  he  had 
a severe  attack  of  vertigo.  He  remained  liable  to  attacks  of  giddiness 
thereafter,  in  wliich  he  had  to  grasp  neighbouring  objects  for  support. 


SOME  ALARMING  SEIZURES  301 

The  attacks  were  steadily  diminishing  in  severity.  His  blood-pressure 
was  230*140.  I have  never  convinced  myself  that  hyperpiesia  itself 
(apart  from  a vascular  lesion)  could  cause  true  vertigo.  In  a long 
scries  of  my  cases  of  vertigo  a normal  or  low  blood-pressure  was  found 
to  be  more  common  than  o high  one.  In  this  case,  however,  I surmise 
that  the  high  blood-pressure  may  have  been  indirectly  responsible 
by  causing  a local  vascular  accident. 

Case  7.  A young  man  who  had  undergone  a great  deal  of  domestic 
strain  for  a number  of  years,  lost  his  mother  suddenly.  On  the  day 
before  the  funeral,  and  again  on  the  morning  of  the  funeral,  he  awoke 
with  nausea  and  intense  giddiness,  the  fireplace  appearing  to  revolve 
to  the  right.  There  were  no  physical  signs  of  disease,  and  in  this  case 
no  deafness  or  tinnitus,  and  there  was  no  history  of  migraine  or 
tobacco  excess.  He  had  always  been  able  to  make  his  right  Eusta- 
chian tube  ‘click’.  Here  the  evidence  for  an  aural  contribution  was 
minimal,  and  I concluded  tliat  emotional  stress  was  the  predominant 
factor. 

Case  8.  A professional  man,  aged  54,  who  had  been  under  my  care 
4 years  previously  for  a duodenal  ulcer,  came  to  see  me  much  exer- 
cised about  symptoms  of  quite  another  kind.  For  C months  he  had 
noticed  increasing  deafness  in  the  right  ear.  One  day  he  suddenly 
collapsed  with  intense  giddiness  and  violent  vomiting,  and  thought 
that  he  might  die  in  the  attack.  He  had  to  be  carried  home,  and 
remained  ill  all  day.  Four  other  attacks  followed  in  the  next  few 
weeks.  He  was  greatly  relieved  in  his  mind  by  the  reassurance  given. 
Three  months  later  he  reported  that  deafness  had  become  complete 
in  the  affected  ear,  and  that  he  no  longer  had  any  giddiness. 

I could  recount  the  histories  of  many  other  cases  of 
vertigo  in  which  anxiety  and  apprehension  were  much  in 
evidence,  leading  in  some  to  a bedridden  invalidism. 
Whatever  other  contributory  measures  or  treatment  are 
employed,  I have  again  and  again  been  impressed  with  the 
value  of  a simple  explanation  and  a full  reassurance.  Dis- 
abuse your  patient  of  all  idea  of  ‘strokes’  or  of  cerebral  or 
heart  disease,  and  you  will  have  given  him  a valuable  helping 
hand.  There  is  no  specific  medical  treatment  of  the  ear 
disease,  and  the  cases  suitable  for  treatment  by  the  neuro- 
logical surgeon  must  remain  in  a minority  and  be  selected 
with  the  most  exclusive  care.  There  is  the  more  reason, 
therefore,  to  concern  ourselves  with  the  associated  factors 
in  the  management  of  these  cases. 


302 


SOME  ALARMING  SEIZURES 


Vasovagal  Attacks  (Gowers’s  Syndrome) 

I have  mentioned  the  sense  of  impending  death  as 
an  occasional  symptom  of  vertigo.  In  vasovagal  attacks 
(Gowers’s  syndrome)  it  is  one  of  the  most  constant  and  quite 
the  most  urgent  and  dreaded  of  symptoms.  These  attacks 
affect  adults  of  either  sex  and  any  age;  they  are  more  fre- 
quent in  women  than  in  men.  In  my  experience  the  victims, 
almost  without  exception,  have  been  affected  simultaneously 
by  a minor  cause  of  general  physical  ill  health  and  by  some 
anxiety  or  mental  stress.  As  with  vertigo  and  fainting,  but 
for  an  even  more  imperative  reason,  the  anxiety  engendered 
by  the  attacks  themselves  is  a strong  perpetuating  factor. 
The  attacks  ‘come  out  of  the  blue’,  and  may  last  minutes, 
or  half  an  hour,  or  for  longer  periods.  They  leave  a sense  of 
prostration  afterwards.  A visceral  disturbance,  such  as 
vomiting  or  diarrhoea,  a bowel  wash-out,  or  an  oesophageal 
or  intestinal  spasm  has  sometimes  precipitated  the  seizure, 
but  no  such  disturbance  can  be  traced  in  the  majority  of 
cases. 

The  chief  complaint  is  of  'a  sense  of  dying* — not  a fear  of 
death,  which  is  sometimes  even  desired,  so  intolerable  is  the 
distress  of  the  attacks.  I have  sat  by  the  bedside  and  been 
assured  by  a patient  that  this  time  the  end  had  come.  In 
other  cases  of  a minor  kind  a sense  of  ‘something  dreadful 
about  to  happen  of  * fading  away  of  * floating  in  space  ’, 
or  a peculiar  ‘sense  of  unreality’  are  described.  There  is 
a complaint  of  profound  malaise,  of  coldness,  sometimes 
of  shivering  or  trembling,  and  of  heaviness,  immobility,  or 
powerlessness  in  the  limbs,  and,  in  these  circumstances, 
patients  have  told  me  that  even  if  a cup  of  restorative  were 
within  reach  they  would  be  unable  to  lift  a hand  to  take  it 
to  their  lips.  This  immobility  is  strongly  reminiscent  of  the 
frozen  powerlessness  observed  in  the  rabbit  ‘fascinated’  by 
the  stoat  or  snake,  and  one  patient,  who  had  seen  an  animal 
in  this  state,  was  forcibly  reminded  of  the  incident  by  her 
own  symptoms.  Praecordial  or  substemal  discomfort,  or 
genuine  pain  spreading  into  the  left  side  of  the  neck  and 
down  the  left  arm,  or  a sense  of  constriction  in  the  chest  is 


SOME  ALARMING  SEIZURES  308 

common,  and  tingling  in  the  finger-tips  and  sometimes  true 
tetanic  spasms  are  also  described.  To  observers  the  patient 
looks  very  ill  and  pale,  and  may  be  cold  to  the  touch.  Even 
medical  men  have  been  deceived,  and  thought  that  death 
was  imminent.  The  pulse  may  be  rapid  or  very  slow.  In 
one  case  of  mine  it  fell  on  occasion  to  36  and  once  even  to 
19  to  the  minute.  Sometimes  the  general  symptoms,  some- 
times the  cardiac  symptoms,  predominate,  but  the  ‘angor 
animi’  is  rarely  absent.  These  attacks  are  often  diagnosed 
erroneously  as  ‘heart  attacks*.  Some  of  them  do,  indeed, 
closely  simulate  angina  pectoris.  Many  of  the  so-called 
pseudo-anginas  in  women  and  younger  subjects  are  ex- 
amples of  Gowers’s  syndrome.  As  a rule  consciousness  is 
retained,  but  occasionally  it  is  lost,  and  when  this  occurs  it 
is  for  much  longer  periods  than  in  the  case  of  an  ordinary 
faint. 

Case  0.  A young  -woman,  previously  healthy  and  placid,  under- 
went an  operation  for  appendicitis.  During  convalescence  she  deve- 
loped almost  every  morning  a pain  across  the  abdomen,  followed  by 
a bowel  action.  On  10  or  12  occasions  this  was  succeeded  by  tachy- 
cardia, feelings  of  deadness  or  numbness  in  both  arms,  especially  in 
the  left,  generalized  tremor,  and  a most  acute  6ense  of  dying.  She 
then  recalled  that  she  had  twice  experienced  somctliing  similar  before 
the  appendicectomy.  With  reassurance  nnd  general  treatment  she 
quickly  outgrew  the  attacks. 

Case  10.  A medical  man,  aged  38,  who  was  recently  convalescent 
from  a gastric  haemorrhage  and  had  experienced  the  sensations 
accompanying  ordinary  faintness,  took  a rather  large  dinner  of  eggs 
and  spinach.  This  was  followed  by  feelings  of  fullness.  He  then 
became  faint,  but  in  spite  of  lying  flat  on  the  ground  the  feelings  grew 
worse.  The  attack  lasted  fully  half  an  hour.  There  was  no  loss  of 
consciousness.  The  patient  thought  he  was  dying,  and  60  did  his 
wife.  ‘He  looked  ghastly  \ and  it  was  not  unnaturally  assumed  that 
he  had  had  a further  haemorrhage.  At  the  end  of  half  an  hour  there 
was  a shivering  attack.  I saw  him  a few  minutes  later,  when  he  was 
warm  again,  but  still  very  pale.  His  pulse-rate  was  72  to  80;  there 
was  no  haemorrhage. 

In  this  case  there  W3s  no  praecordial  distress.  To  the  patient  and 
medical  friends  who  were  present  the  episode  was  something  different 
from  an  ordinary  faint,  a state  in  which  angor  animi  is  not  described, 
and  the  symptoms  are  generally  of  short  duration  or  quickly  followed 
by  loss  of  consciousness. 


004  SOME  ALARMING  SEIZURES 

Case  II.  A woman,  aged  51,  of  nervous  temperament,  and  of  the 
anaemic,  flabby  type,  sent  for  her  doctor  urgently  one  night  on 
account  of  epigastric  and  substema!  pain.  She  thought  she  was  going 
to  die.  She  looked  ‘ashy’  white,  and  had  a very  slow  pulse;  6hc  re- 
covered slowly,  the  whole  episode  lasting  about  one  hour.  She  gave  a 
confused  account  of  previous  attacks,  some  of  which  sounded  dyspep- 
tic, while  in  some  she  experienced  praeeordial  and  left  arm  pain  ns  a 
result  of  effort  or  during  a game  of  bridge.  In  these  attacks  she  had  a 
4 feeling  in  the  throat  and  difficulty  in  drawing  her  breath’.  She  had 
a sharp  aortic  second  sound.  Her  blood -pressure  was  1 CO-1 00.  Many 
members  of  her  family,  including  a sister,  were  reported  to  have  died 
suddenly.  The  decision  as  between  true  angina  pectoris  and  Gowers’s 
syndrome  was  here  a difficult  one.  Later  she  was  re-examined,  and 
on  two  occasions  a normal  electrocardiogram  was  obtained.  She  re- 
mained fairly  well  during  the  next  year,  except  for  ‘indigestion’,  and 
experienced  no  pain  or  dyspnoea  on  walking.  She  was  then  seized 
with  a severe  attack  of  stomach  pain  wlrilc  driving  in  a car,  and  was 
taken  to  a chemist’s  shop,  but  becoming  worse  was  moved  to  a 
doctor’s  house.  Here  the  doctor,  seeing  her  for  the  first  time,  made  a 
confident  diagnosis  of  angina.  I saw  her  shortly  afterwards,  and  was 
much  more  in  favour  of  Gowers’s  syndrome  than  before,  and  con- 
sidered anaemia  and  anxiety  again  as  underlying  causes.  Her  blood- 
pressure  was  now  140-05.  A little  later  her  own  doctor  was  called, 
on  more  than  one  occasion,  to  sec  her  in  attacks  in  which  the  sense 
of  impending  death  was  predominant,  and  pain  quite  a secondary 
symptom.  There  was  now  an  additional  complaint  of  ‘stiffness  in 
the  hands  and  feet’.  These  attacks  occurred  at  rest  in  bed,  and  were 
so  unlike  true  angina  that  the  alternative  opinion  was  finally  adopted, 
and  treatment  modified  accordingly. 

Further  descriptions  of  vasovagal  seizures  are  given  in 
Chapter  V. 

It  is  noteworthy  that  the  same  sense  of  constriction  in  the 
chest  and  angor  animi  which  these  patients  describe  can 
occur  in  anaphylactic  shock,  and  that  they  may  also  be 
evoked  by  too  large  a dose  of  adrenaline  given  hypodermi- 
cally. In  either  case  it  seems  reasonable  to  suggest  that  an 
abrupt  fluctuation  in  the  blood-pressure  is  an  operative 
cause.  In  some  cases  vasovagal  attacks,  like  migraine,  occur 
at  intervals  throughout  a long  life,  and  although  patients 
come  to  realize  that  they  will  survive  them,  the  sense  of 
dying  or  angor  animi  is  not  one  whit  diminished  at  the  time. 

I have  seen  the  fear  and  misery  engendered  by  the  attacks 
in  women  of  frail  constitution  or  hysterical  type  lead  to 


SOME  ALARMING  SEIZURES  395 

bed-ridden  invalidism,  but  most  patients  continue  to  go 
about  their  affairs,  and  many,  presumably,  outgrow  the 
attacks  altogether,  or  experience  them  in  diminishing 
degree. 

The  vasovagal  attacks  of  Gowers  are  by  no  means  as  rare 
as  they  are  sometimes  supposed  to  be.  I have  collected  82 
cases  in  the  course  of  private  practice,  as  compared  with  72 
of  labyrinthine  vertigo,  and  218  of  migraine  (all  types). 
They  are  commonly  labelled  as  ‘heart  attacks’,  ‘pseudo- 
angina’,  ‘ nerves  ’,  and  ‘ anxiety  attacks  ’,  but  they  are  so  true 
to  type,  in  respect  of  both  their  subjective  and  their  objec- 
tive phenomena,  that  these  varied  and  looser  nomenclatures 
should  not,  in  my  belief,  be  sanctioned.  They  are  at  least  as 
deserving  of  separate  classification  as  fainting,  epilepsy, 
migraine,  and  vertigo,  with  which  they  also  bear  definite 
relationships. 

Summary 

We  find,  then,  that  all  of  these  seizures  tend  to  occur  in 
persons  of  particular  type  or  temperament  ,*  they  are  parox- 
ysmal and  intermittent,  ‘coming  out  of  the  blue’ ; they  are 
of  limited  duration ; they  are  associated  with,  and  leave  in 
their  train,  no  structural,  nervous  or  visceral  damage ; they 
tend  to  create  grave  anxiety  and  apprehension;  they  are 
more  likely  to  develop  at  times  of  general  unfitness,  whether 
of  a physical  or  a mental  kind ; and,  in  no  small  degree,  they 
seem  to  merge  with  one  another  and  to  possess  common 
clinical  features  and  aetiological  characters.  Just  as 
migraine  has  relationships  with  epilepsy  and  may  occasion- 
ally be  replaced  by  an  epileptic  seizure,  so  also  it  may  take 
on  a vertiginous  character  and  remind  us  of,  or  be  mistaken 
for,  labyrinthine  vertigo.  Labyrinthine  vertigo  in  turn  may 
be  accompanied  by  the  collapse  and  feeling  of  impending 
death  which  we  have  seen  to  be  leading  symptoms  of  the 
vasovagal  attack.  I have  several  case-histories  of  patients 
who  were  afflicted  both  with  migraine  and  with  vasovagal 
attacks.  Bad  bouts  of  migraine,  vertigo,  and  vasovagal 
distress  are  all  liable  to  be  followed  by  feelings  of  prostration 
enduring  for  a day  or  more,  and  the  two  first  are  sometimes 


000  SOME  ALARMING  SEIZURES 

followed  by  a profound  sleep.  The  vasomotor  phenomena  of 
fainting — namely,  coldness  and  pallor — are  common  to  all 
tliree,  and  in  all  three  loss  of  consciousness  may  very  occa- 
sionally occur.  Whatever  the  nature  of  the  neuronic  cyclone 
we  find  grounds  for  arguing  that  these  various  manifesta- 
tions represent  disturbances  of  a similar  kind,  but  varying 
in  degree  and  occurring  at  different  levels  in  the  sensorium. 

Wilks  [2]  long  ago  remarked:  ‘It  is  undoubtedly  true  that 
there  is  not  a single  organic  disease  of  the  nervous  system 
which  may  not  be  simulated  by  a functional  and  curable 
one.’  Hemiplegic  migraine  has  its  counterpart  in  organic 
hemiplegia.  The  vertiginous  episodes  have  their  counter- 
parts in  cerebral  and  cerebellar  disease.  I have  elsewhere 
given  reasons  for  supposing  that  vasovagal  attacks  arc  ex- 
pressive of  a medullary  storm,  and  the  sense  of  impending 
death  may  actually  occur  with  organic  lesions  which  involve 
or  embarrass  the  medulla  oblongata  [3,  4], 

In  the  handling  of  cases  in  which  fear  and  apprehen- 
sion are  an  inevitable  accompaniment  it  is  clearly  a grave 
error  to  suggest  a diagnosis  of  organic  disease,  and  yet,  their 
true  nature  having  passed  unrecognized,  it  is  by  no  means 
rare  for  vertigo  and  the  stranger  variants  of  migraine  to  be 
ascribed  to  cerebral  disease  and  for  vasovagal  attacks  to  be 
called  ‘cardiac’.  A general  regulation  of  the  patient’s  way 
of  life,  the  discovery,  and,  so  far  as  possible,  the  elimination 
of  adverse  physical  or  psychological  influences,  and  the 
judicious  employment  of  sedatives  such  as  bromides  and 
luminal  to  ‘damp  down ’ native  irritability,  play  a reason- 
able part  in  treatment. 

In  migraine  a strict  exclusion  of  eggs,  chocolate,  and  fats 
from  the  dietary  is  often  rewarded.  More  exercise  and  a 
moderation  of  mental  activities  commonly  help.  But  what- 
ever measures  we  employ  it  is  of  the  first  importance  to 
examine  carefully,  to  explain  simply,  and  to  reassure  fully, 
and  so  to  remove,  so  far  as  may  be,  the  crippling  element  of 
doubt  or  dread.  In  dealing  with  these  cases  we  are  repeatedly 
reminded  that  the  study  of  the  patient  as  a whole,  and  of  his 
environment  and  his  family  history,  by  completing  our 
diagnosis  or  * thorough  knowledge  ’ of  his  malady,  gives  us 


SOME  ALARMING  SEIZURES  397 

the  surest  guidance  in  our  choice  of  measures  for  relief, 
whether  these  be  of  a physical  or  of  a psychological  kind. 
Even  when  ultimate  pathologies  remain  obscure  it  is  a 
matter  for  comfort  that  it  lies  within  our  power  to  recognize 
that  some  of  the  more  alarming  episodes  of  medical  prac- 
tice need  not,  in  fact,  occasion  any  fear  of  an  unhappy 
ending. 

REFERENCES 

1.  Gowers,  Sir  William:  The  Borderland  of  Epilepsy,  1007. 

2.  Wilks,  Sir  Samuel:  Lectures  on  Diseases  of  the  Nervous  System, 

1883. 

3.  Ryle,  J.  A.:  Guy's  Hospital  Reports,  1025,  Ixxviii.  371. 

4.  Lancet,  3931,  J.  737. 


OF  NOSOPHOBIA 


Few  would  deny  that  fear  may  become  or  engender  disease. 
It  might  almost  be  described  as  the  great  pandemic  malady. 
I have,  alternatively,  referred  to  it  as  one  of  the  two  great 
primary  symptoms.  Pain  is  the  other  one.  They  are,  in  fact, 
whatourpatientschiefiy  bringtous.  Fcarand  anxiety  (which 
may  be  regarded  as  low-grade  continuing  fear)  are  probably 
commoner  symptoms  even  than  pain  although  they  remain 
more  frequently  unspoken.  Fears  and  anxieties  may  be 
reasonable  or  unreasonable,  but  they  do  not  lack  a cause. 
They  may  be  related  to  external  circumstances,  to  domestic 
or  economic  difficulties,  to  bombs,  or  to  the  international 
situation.  But  they  may  be  related  also,  and  are  probably 
more  frequently  related,  to  the  patient’s  internal  economy 
and  his  private  thoughts  about  it;  to  his  symptoms  and 
their  possible  import ; to  the  effects  which  illness  or  accident 
may  have  on  prospects,  activity  or  earning  power;  to  ideas 
of  pain  and  suffering  and  their  tolerability;  and  to  ideas  of 
death  and  dying.  Many  of  our  patients,  indeed  the  majority, 
who  harbour  fears  or  anxieties  about  themselves  have  no 
structural  disease  although  they  majr  have  definite  physical 
symptoms.  Anxiety  itself  may  be  a main  cause  of  these 
symptoms  and  is  in  turn  aggravated  by  them.  In  such  case 
Anxiety  becomes,  in  fact,  the  diagnosis  or  the  real  disease. 
But  we  sometimes  tend  to  forget  that  patients  with  organic 
maladies  and  injuries  also  harbour  fears  and  apprehensions 
and  then,  because  they  show  no  outward  signs  of  neurosis, 
their  unspoken  troubles  (often  of  a degree  and  kind  to  retard 
progress  or  aggravate  suffering)  remain  uneomforted. 

Tee  Meaning  of  Nosophobia  • 

Among  the  twelve  diagnoses  which  appear  most  fre- 
quently in  my  case-records  Anxiety  comes  second  on  the 
list.  In  four  of  the  other  eleven,  including  the  first  on  the 
list,  it  is  probably  an  important  causal  or  contributory 


OP  NOSOPHOBIA  390 

factor.  But  there  is  no  disease,  whether  grave  or  trivial,  in 
which  fear  may  not  sometimes  play  a part.  Nosophobia  is 
derived  from  the  two  Greek  words  vocro?  meaning  disease 
and  rf>ofios  meaning  fear.  It  has  come  to  be  applied  particu- 
larly to  a morbid  dread  or  neurotic  fear  of  disease,  but  there 
is  no  reason  why  it  should  have  this  limited  meaning  and  I 
shall  here  employ  it  in  its  widest  sense.  It  can  then  be  used 
to  describe  a fear  of  an  existent  or  a non-existent  disease, 
of  a disease  which  a patient  has  or  thinks  he  has  or  fears  he 
may  acquire,  or  of  the  consequences  which  disease  or  injury 
may  bring  to  him  or  those  dependent  on  him. 

"While  alknving  that  there  are  phlegmatic,  insensitive, 
and  care-free  individuals  who  make  light  of  their  physical 
disabilities  we  would  do  well  to  presume  the  presence  of 
some  degree  of  anxiety  in  nearly  every  general  medical  case 
reporting  for  diagnosis  and  advice;  in  most  acute  illnesses  in 
which  consciousness  is  not  dimmed;  in  most  bad  surgical 
cases  and  accidents  and  woundings  in  which  the  mind  is 
unclouded  by  the  effects  of  shock  and  haemorrhage;  in 
most  cases  of  sudden  bleeding  before  serious  weakness 
supervenes ; in  most  conditions  calling  for  the  knife,  for  here 
the  fear  of  the  operation  and  the  anaesthetic  aids  and  abets 
the  fear  occasioned  by  the  illness;  and  in  quite  a large 
proportion  of  other  conditions  which  to  us  seem  very  trivial. 
Can  any  of  us  say  that  we  have  submitted  to  gas  for  a dental 
extraction  or  the  incision  of  a whitlow  without  a passing 
flicker  of  anxiety  ? Can  any  of  us  maintain  that  transient 
pains,  discomforts,  or  rashes  have  never  created  apprehen- 
sion in  our  thought? 

By  comforting  explanation  and  reassurance,  by  mini- 
mizing fears  when  there  is  no  reason  for  them  to  be  other- 
wise than  minimal,  by  abolishing  uncertainties  about  organic 
lfiness  in  the  minds  both  of  patients  and  their  refafives 
whenever  possible,  be  the  illness  heart  disease,  pneumonia, 
phthisis,  appendicitis,  cancer,  or  measles,  we  can  bring 
genuine  and  sometimes  surprising  benefits  to  the  mind  and 
to  the  body  through  the  mind.  By  demonstrating  and 
relieving  the  fear  factor  in  the  ‘functional  ’ case  we  can  often 
remove  or  greatly  benefit  the  disease  itself.  One  has  only  to 


400  OF  NOSOPHOBIA 

recall  facial  expressions  of  relief  or  halting  words  of  thanks 
or  even  sudden  changes  for  the  better,  which  are  within 
the  experience  of  every  doctor,  to  feel  sure  that  comfort  of 
this  kind,  even  if  it  is  not  always  lasting,  is  an  essential 
therapeutic  contribution.  The  too-frequcnt  omission  of  the 
encouraging  word  or  the  pat  on  the  shoulder  is  not,  let  me 
insist,  to  be  ascribed  to  hardness  of  heart  or  any  callous 
attitude,  but  simply  to  a failure  to  realize  that  such  gestures 
are  needed  or  to  a preoccupation  with  symptoms  which 
seem  so  far  physical  as  to  call  only  for  physical  methods  of 
treatment.  Even  in  the  resuscitation  ward  after  an  air-raid 
I have  sometimes  noticed  two,  three,  or  more  people  engaged 
on  a fracture  or  a wound  and  giving  it  every  care  and 
attention,  but  without  one  of  them  pausing  to  spend  a 
moment  with  the  patient  afterwards  to  tell  him  that ‘It’s 
not  too  bad,  old  chap’,  or  ‘We  shall  be  able  to  save  your 
limb’,  or  to  the  chilled  and  frightened  girl  ‘We’ll  soon  have 
you  warmed  up  and  feeling  better’.  It  takes  no  time  and  it 
means  so  much  and,  having  escaped  one  terror,  the  poor 
things  ought  not  to  be  allowed  to  suffer  a moment  of 
unnecessary  dread.  We  become  so  familiar  with  the  general 
appearances  and  course  and  prospects  of  common  diseases 
and  so  interested  in  local  pathologies  that  we  tend  to  forget 
the  minds  and  the  prevailing  ignorance  in  the  minds  of  our 
patients,  and  also  that  many  of  them  are  too  timid  or 
incoherent  to  ask  the  very  question  that  would  give  us  the 
opening  we  need  to  set  their  hearts  at  rest.  So  many 
medical  students  develop  fears  of  disease  during  their 
apprenticeship  that  it  is  curious  that  they  should  so  readily 
overlook  their  influence  or  underestimate  their  prevalence 
in  later  life  in  others. 

We  should  remember  too  the  many  agencies  at  work 
which  foster  a morbid  interest  in  disease — the  daily  and 
still  more  the  Sunday  papers,  the  advertisements  of  patent 
medicines,  the  advice  or  gloomy  talk  of  friends,  the  know- 
ledge of  the  illnesses  and  deaths  of  relatives.  Although  in 
times  of  health  these  may  be  the  pepper  and  salt  of  life  for 
some  gossiping  folk,  when  sickness  comes  it  is  their  smart 
which  prevails  rather  than  their  condiment  effect. 


OF  NOSOPHOBIA  401 

Types  of  Nosophobia 

Let  us  now  consider  some  of  the  more  important  varieties 
of  this  fear  of  disease,  of  the  prevalence  of  which  we  need 
entertain  no  doubts. 

(1)  Nosophobia  may,  in  accordance  with  the  common 
usage  of  the  term,  take  the  form  of  a quite  unreason- 
ing fear  of  a particular  disease  from  which  the  patient 
does  not,  in  fact,  suffer,  or,  alternatively,  of  an  un- 
reasoning fear  that  he  may  acquire  it. 

The  victims  of  this  form  of  the  malady  are  usually 
endowed  with  psychoneurotic  or  psychotic  personalities. 
Syphilophobia  is  a well-recognized  example.  It  may  afflict 
both  those  who  have  exposed  themselves  to  a risk  of  infection 
and  those  who  have  never  once  incurred  it.  A sense  of  guilt 
dependent  on  faulty  or  puritanical  upbringing  may  play  a 
part  in  such  cases.  The  anxiety  tends  to  become  fixed  and 
magnified  into  a central  obsession  and  may  be  extremely 
difficult  to  dislodge.  Negative  blood  tests  fail  entirely  to 
convince  or  satisfy  the  unhappy  mind  and  serious  mental 
derangement  may  follow.  Phobias  almost  as  resistant  may 
be  developed  for  cancer,  but  the  majority  of  cancer  phobias 
are  of  a much  more  manageable  order  and  they  do  not  involve 
feelings  of  taint  or  unworthiness. 

(2)  Another  form  of  nosophobia  is  the  dread  of  disease  as 
a whole  or  of  some  common  group  of  diseases  such  as 
the  infectious  or  contagious  group. 

This  tends  to  afflict  nervous  people  with  a smattering  of 
knowledge  about  bacteria  or  the  children  of  anxious  parents 
who  have  compelled  them  to  lead  unduly  sheltered  lives. 
Medical  students  are  often  the  temporary  victims  of  disease 
phobias  of  this  kind.  They  may  lead  to  excessive  washing 
of  the  hands  or  to  misinterpretations  of  trivial  symptoms 
which 'become  so  far  magnified  as  to  suggest  one  or  more 
of  the  graver  pathologies  which  find  illustrations  in  the 
museum  and  the  wards  and  about  which  the  text -books  are 
so  graphic.  These  fears,  too,  are  unreasonable.  Although  they 
may  be  said  to  have  some  foundation  in  experience  they 

d d 


402  OF  NOSOPHOBIA 

remind  us  that  a little  knowledge  can  be  a dangerous 
thing.  They  are  usually  quickly  curable  by  a careful  overhaul 
and  a sensible  talk.  It  is  not  wise  to  laugh  at  them.  A 
student  came  to  see  me  some  years  ago  convinced  that  he 
had  a cancer  of  the  rectum  because  he  believed  himself  to  be 
getting  thin.  He  carried  his  own  photograph  about  with  him 
and  frequently  compared  it  with  his  face  in  the  glass.  I 
examined  and  reassured  him  thoroughly,  reminding  him 
that  loss  of  weight  in  rectal  carcinoma  was  only  likely  to 
develop  in  the  later  stages  and  to  the  tune  of  recognizable 
symptoms  and  signs,  and  finally  appropriated  his  photo- 
graph. When  last  heard  of  he  was  hard  at  work  in  a busy 
practice  and,  let  us  hope,  relieving  other  patients  of  their 
fears. 

(3)  A third  and  by  far  the  commonest  form  of  nosophobia 
is  that  engendered  by  more  or  less  defined  but  un- 
explained physical  symptoms. 

Internal  pains  may  suggest  cancer  in  middle  life.  Pain 
in  the  right  iliac  fossa  promotes  fears  of  appendicitis,  not 
only  in  patients,  but  also  in  their  doctors,  and  has  resulted 
in  the  removal  of  countless  innocent  organs,  often  enough 
for  symptoms  whose  closer  analysis  would  scarcely  have 
been  consistent  with  a local  inflammatory  lesion.  Coughs 
and  sweating  and  loss  of  weight  suggest  tuberculosis. 
Vertigo  and  nphasic  migraine  suggest  strokes.  A fear  of 
going  out  of  their  minds  is  common  in  the  psychoneurotics. 
Fainting  suggests  heart  disease,  of  which  it  is,  in  fact, 
very  rarely  a symptom.  The  vasovagal  attacks  of  Gowers 
suggest  angina  pectoris  or  heart  failure  with  particular 
aggravation  by  the  strange  physical  sense  of  dying  which 
may  accompany  them.  In  all  such  cases  a confident 
diagnosis  and  explanation  are  the  first  contribution  to 
treatment  whatever  other  measures  may  be  employed  to 
combat  the  whole  disorder  or  to  correct  an  emotional 
situation.  These  phobias  are  more  reasonable.  They  are 
based  upon  a wrong  interpretation  of  symptoms,  it  is  true, 
but  often  of  symptoms  which  have  taken  time  to  unravel 
and  may  have  provided  the  medical  profession  with  diffi- 


OF  NOSOPHOBIA  403 

eulties  and  indecisions  which  do  not  escape  the  notice  of 
the  intelligent  patient. 

(4)  Nosophobia  can  often  be  traced  to  misconceptions 
for  which  the  doctor  is  to  blame,  to  erroneous  or 
incomplete  diagnoses,  to  a simple  failure  on  his  part 
to  explain  and  reassure  because  he  had  not  appreci- 
ated the  patient’s  state  of  ignorance  or  apprehension, 
or  to  a needlessly  gloomy  or  guarded  prognosis,  or  to 
forgetting  to  give  a prognosis  at  all. 

Fears  encouraged  by  omissions  in  this  way  are  by  no 
means  rare.  Other  fears  may  originate  in  the  unguarded 
public  pronouncements  of  medical  men  which  must  then  be 
accounted  sins  of  commission.  Whenever  possible  we  should 
tell  our  patients  that  they  are  going  to  get  better,  or,  at 
least,  that  they  are  doing  well,  or,  even  when  we  are  dubious 
about  the  issue,  that  they  are  fighting  a good  fight  and  that 
everyone  is  out  to  help  them.  Those  physicians  and  surgeons 
have  always  been  the  most  successful  who  have  best 
inspired  hope  and  courage  in  the  sick-room. 

(5)  Finally,  with  the  fear  of  disease  and  its  pains  and 
penalties,  we  must  couple  the  particular  fear  of  death 
which  illness  cannot  fail,  in  certain  circumstances,  to 
promote. 

Busy  with  the  management  of  a case  and  with  our  own 
anxieties  it  is  strangely  easy  to  omit  the  necessary  word  of 
encouragement  to  a victim  of  sudden  haemorrhage  or  other 
urgent  symptoms,  although  the  whole  atmosphere  of  the 
sick-room  and  the  expressions  on  friendly  faces  unable  to 
conceal  care,  not  to  mention  the  disturbing  symptoms 
themselves,  must  appear  as  danger  signals.  Oxygen  cyl- 
inders should  be  kept  out  of  view  when  not  in  use,  for 
oxygen,  quite  wrongly,  suggests  only  desperate  situations 
to  the  lay  mind.  Curiously  enough  the  terrible  feeling  ( not 
fear)  of  impending  death  which  is  experienced  by  the 
victims  of  vasovagal  attacks  and  vertiginous  seizures  and 
anaphylactic  episodes  and  in  some  cases  of  angina  pec- 
toris (the  angor  animi  of  the  older  physicians)  is  rarely,  if 


401  OF  NOSOPHOBIA 

ever,  encountered  in  those  whose  lives  nre  immediately  in 

jeopardy. 

Let  us  pass  now  to  some  case-histories  illustrative  of  these 
various  types  of  fear. 

Case  1.  Syphilophobia.  A man,  aged  35,  -who  had  been  a prisoner 
in  German  hands  during  the  1014-18  war  for  four  years,  was  treated 
during  that  period  for  a urethritis,  but  denied  exposure.  After  his 
return  he  was  pronounced  free  from  infection  and  his  WJR.  was  also 
negative.  In  the  course  of  the  next  few  years  he  had  much  sorrow 
and  Joss,  his  first  wife  dying  in  childbirth  and  his  second  from  a 
cerebral  abscess.  A year  before  I saw  him  his  urethral  discharge 
reappeared.  He  was  treated  without  a bacteriological  examination. 
My  notes  state  that  ‘he  has  developed  a persistent  obsession  that 
he  has  syphilis.  He  complains  of  pains  in  the  sacrum,  the  perineum, 
the  neck,  the  eyes,  and  under  the  finger  nails,  of  flatulence  and 
insomnia  and  has  lost  a stone  in  weight.’  I discovered  a to-and-fro 
aortic  murmur,  which  was  rather  disconcerting,  refrained  from  dis- 
cussing it  with  him,  and  admitted  him  to  hospital  for  further  ins  estima- 
tion with  a reassuring  forecast.  There  we  obtained  another  negntise 
blood  1VJI.  and  also  a negative  urethral  smear,  and,  better  still,  a 
history  of  three  attacks  of  rheumatic  fever  in  boyhood.  He  was  at 
the  time  much  comforted  by  these  reports  and  a vigorous  reassur- 
ance, but  I have  not  heard  how  he  fared  subsequently.  The  back- 
ground of  a long  imprisonment  and  his  domestic  tragedies  probably 
played  a large  part  in  maintaining  his  anxiety  of  mind  and  condi- 
tioning the  phobia  into  which  it  had  crystallized. 

Case  2.  Syphilophobia.  A nervous  Jew,  aged  SI , married  and  witJj 
children,  developed  warts  on  the  hands  and  a friend  told  him  that 
they  were  venereal.  He  was  terrified  and  began  to  be  physically 
‘side  with  worry’.  Pains  in  the  joints  followed  and  then  he  thought 
he  had  a stricture.  He  lost  energy  and  all  interest  in  his  business 
and  dropped  two  stone  in  weight.  An  opportunity  of  dealing  with 
his  friend  would  have  been  welcome. 

Case  3.  Infection  phobia.  Many  of  us  must  have  had  transitory' 
fears  of  septic  or  venereal  infection  from  patients  during  our  student 
days  or  afterwards.  One  contemporary  of  mine,  now  dead  of  a disease 
which  he  never  feared,  developed  what  amounted  to  a compulsion 
neurosis  in  regard  to  the  possibility  of  infection.  Having  washed 
in  the  hospital  he  would  wash  again  in  the  students’  club  before  his 
meals,  open  the  swing  doors  with  his  elbows,  eat  his  College  lunch, 
and  then  flame  the  end  of  his  cigarette  before  putting  it  in  his  mouth. 
The  unhygienic  condition  of  the  kitchens  and  dining-hall  in  those  days 
and  the  fact  that  the  food  and  the  utensils  must  have  passed  through 
many  unwashed  hands  before  it  reached  him  did  not  seem  to  worry 


OF  NOSOPHOBIA  405 

him.  The  fact  that  hundreds  of  men  risked  dining  in  College  year  after 
year  and  took  none  of  his  precautions  and  yet  acquired  no  fell  disease 
also  failed  to  impress  him.  His  nosophobia  was  distinctly  unreason- 
able. 

Case  4.  Illness  and  fear  engendered  by  knowledge  of  disease  in 
others.  In  the  course  of  one  morning's  out-patients  recently  we  had 
two  patients  with  symptoms  resulting  from  this  cause.  One  was  a 
healthy  girl  of  18,  about  whose  heart  some  anxieties  had  been  enter- 
tained in  childhood,  although  she  then  had  no  symptoms.  She  had 
recently  complained  of  momentary  stabbing  pains  in  the  sub-mam- 
mary region  which  did  not  at  all  suggest  cardiac  disease  and  the 
examination  was  negative.  Her  mother  then  told  us  that  the  girl 
had  been  working  for  a lady  with  heart  disease.  The  association  of 
a past  suspicion  of  cardiac  trouble  and  the  spectacle  of  real  trouble 
in  another  provided  the  mental  basis  for  the  symptoms.  The  other 
patient  was  a young  married  woman  complaining  of  loss  of  weight, 
sweats,  dry  mouth,  and  multiple  bodily'  pains,  but  without  attendant 
objective  signs  of  disease.  She  freely  admitted  on  questioning  that 
her  symptoms  had  all  dated  from  the  loss  of  a friend  from  pulmonary 
tuberculosis  and  that  she  was  living  in  dread  of  this  disease. 

Case  5.  Nosophobia  due  to  indiscreet  pronouncements  by  medical 
men.  I was  once  consulted  by  two  old  spinster  sisters  who  arrived  in 
a great  state  of  trepidation.  A distinguished  surgeon  had  given  it  as 
his  opinion  that  a diet  consisting  largely  of  vegetable  foods  and  carrots 
would  protect  against  cancer.  They  had  embarked  upon  his  pro- 
gramme, but  it  had  suddenly  occurred  to  them  that  they  might 
have  started  it  too  late  in  life  and  that  the  seeds  of  cancer  might  have 
already  gained  a foothold  1 It  is  not  easy  to  eradicate  a disease 
phobia  when  it  lias  been  prompted  by  a man  supposed  by  the  public 
to  be  vested  with  high  scientific  authority.  Let  us  hope,  nevertheless, 
that  I was  successful  both  in  relieving  their  minds  and  assuring  them 
that  their  tedious  diet  was  not  really  necessary. 

Cancer  Phobia 

Apart  from  its  high  mortality  and,  in  many  cases,  its 
relentlessness,  cancer  has  inspired  fear  in  the  lay  mind 
because  of  its  supposedly  inevitable  association  with  grave 
pain.  We  would  do  our  patients  and  the  public  a real  service 
if  we  were  to  remind  them  more  often,  firstly,  that  cancer  in 
its  early  stages  is  becoming  gradually  more  eradicable  and, 
secondly,  that  it  is  by  no  means  always  a painful  disease; 
that  carcinoma  of  the  stomach,  the  liver,  and  the  bowel,  for 
instance,  can  all  run  a painless  course  (although  we  know 


400  OF  NOSOPHOBIA 

they  do  not  always  do  so),  and  that  when  the  disease  is 
incurable  and  accompanied  by  pain  a great  deal  can  be 
done  to  relieve  that  pain.  There  ore  deaths  more  miserable 
than  many  of  the  cancer  deaths  which  are  not  a source  of 
public  dread — deaths,  for  instance,  from  slowly  progressive 
central  nervous  disease  with  loss  of  speech,  power,  and 
sphincter  control. 

In  the  presence  of  cancer  we  are  always  faced  with  the 
problem  of  whether  to  tell  the  patient  the  diagnosis.  No 
hard  and  fast  rule  can  be  made.  Sensitive  elderly  folk 
whose  days  are  short  can  often  be  spared  the  knowledge. 
Sensitive  younger  folk,  women  especially,  are  better  spared 
it  in  many  cases.  Many  never  ask  us  for  a diagnosis  and  yet 
leave  us  suspecting  that  they  knew  it  all  along.  Men  with 
responsibilities  and  other  brave  people,  both  religious  and 
agnostic,  prefer  to  be  told,  and  it  may  be  our  hard  duty  to 
decide  for  ourselves  from  what  we  know  of  them  that  this 
would,  in  fact,  be  their  preference ; they  are  then,  with  our 
help,  in  a position  to  gather  their  cloak  of  courage  round 
them  and  to  set  their  affairs  in  order.  When  wc  decide  not 
to  tell  dissimulation  may  not  always  be  easy,  but  in  the 
case  of  gastric  and  colonic  cancer  it  is  always  legitimate  and 
not  untruthful  to  speak  of  *a  severe  ulceration’  of  a type 
suitable  or  unsuitable,  as  the  case  may  be,  for  operative 
treatment.  Some  patients  and  especially  women  with  breast 
cancers,  will  conceal  their  disease  until  it  is  far  advanced 
rather  than  be  told  what  they  dread  at  a stage  when  it  is 
amenable  to  treatment.  Such  psychological  peculiarities 
are  puzzling,  but  in  the  individual  case  must  be  viewed  with 
tolerance. 

Cancer  phobia  without  cancer  is,  however,  far  commoner 
than  cancer  phobia  with  cancer.  I have  carefully  perused 
the  notes  of  thirty-one  cases  in  which  cancer  phobia  (with- 
out cancer)  was  the  main  diagnosis.  These  are  a mere  fraction 
of  the  patients  seen  who  harboured  the  fear  in  some  degree. 
There  were  twenty-one  women  and  ten  men.  The  average  age 
was  50,  the  youngest  83  and  the  oldest  75.  Thirteen  were  de- 
scribed as  nervous,  very  nervous,  oras  having  had  a nervous 
breakdown  on  one  or  more  occasions.  The  physical  symp- 


OF  NOSOPHOBIA  407 

toms  complained  of  were  generally  of  a kind  associated 
with  emotional  disorder.  Thus,  fourteen,  with  or  without  a 
specific  mention  of  neurosis,  were  the  victims  of  spastic  colon 
or  other  colonic  discomforts,  of  flatulence,  globus  or  rectal 
spasm,  or  had  had  an  abdominal  exploration.  Two  patients 
had  duodenal  ulcers,  and  two  cholecystitis.  One  had 
hyperpiesia. 

In  six  cases,  all  women,  there  was  a mention  of  sore  or 
dry  tongue  or  mouth  or  of  altered  taste  with  no  evidence  of 
a local  cause  for  the  symptoms.  In  such  cases  I have  come 
to  expect  or  inquire  for  a cancer  phobia.  Is  the  condition 
perhaps  related  to  the  dry  mouth  of  more  acute  anxiety? 
One  case  was  cured  of  the  symptom  and  her  fears  by  the 
interview  and  another  greatly  relieved  by  the  assurance 
given. 

Twelve  patients  in  the  series  had  lost  a near  relative  or 
friend  or  neighbour  from  cancer  or  had  intimate  knowledge 
of  a ease  or  cases.  Two  were  in  the  habit  of  reading  articles 
in  the  papers  or  other  literature  bearing  on  cancer. 

Case  6.  A very  intelligent  middle-aged  layman,  with  expert  know- 
ledge of  hospital  administration,  developed  a troublesome  lumbo- 
sacral pain  after  a blow  in  the  back.  On  a basis  of  his  medical  half- 
knowledge and  a vivid  imagination,  his  age,  the  persistence  of  his 
symptom,  and  a contrast  of  his  present  state  with  his  normally  good 
health,  he  built  up  an  association  which  seemed  to  support  his  fear 
of  cancer.  He  slept  badly  and  lost  a stone  in  weight.  He  saw  several 
doctors.  He  was  cured  by  a single  explanation  and  reassurance. 
Two  years  later  he  was  seen  for  a much  slighter  anxiety  about  his 
heart  and  again  relieved.  Later  he  developed  a duodenal  ulcer  which 
caused  him  no  serious  anxiety  and  responded  to  orthodox  medical 
treatment. 

Case  7.  A spinster,  aged  70,  had  twice  been  treated  successfully 
for  rodent  ulcers.  Her  brother  had  died  of  cancer  of  the  gullet.  Her 
friends  told  her  that  she  was  getting  thin.  She  had  lost  a stone  in 
weight,  but  had  taken  four  years  to  do  so.  She  was  given  to  reading 
literature  about  cancer.  There  were  thus  several  good  causes  for 
her  fears. 

Case  8.  A married  woman,  aged  61,  suddenly  developed  a bitter 
taste  in  her  mouth  and  later  cold  feelings  in  the  body  and  slight  pains 
in  neck  and  shoulders.  She  worried  more  and  more  about  these 
symptoms  and  slept  badly.  Two  distant  relatives  had  recently  died 


40S  OF  NOSOPHOBIA 

of  cancer.  She  had  seen  a doctor,  hut  had  not  been  given  a complete 
overhaul  or  a reassurance  of  the  kind  she  needed.  Eight  months 
later  her  daughter  reported  that  she  had  been  well  from  the  day  of 
the  consultation. 

Case  0.  A nervous  unmarried  woman,  aged  47,  and  passing 
through  the  climacteric,  had  twice  had  a nervous  breakdown  in  earlier 
life.  Her  mother  and  paternal  grandfather  had  died  of  cancer.  Two 
months  previously  she  had  begun  to  worry  and  to  sleep  badly  because 
a friend  of  hers  was  dying  of  cancer.  Her  symptoms  included  pains 
in  the  throat,  rectum,  and  vagina.  Three  years  previously  she  had  had 
n disease  phobia  in  association  with  abdominal  symptoms. 

It  will  be  seen  from  these  histories  that  the  fears  which 
we  unearth  in  our  patients  are  often  by  no  means  unreason- 
able and  that  multiple  factors  arc  often  at  work.  We  do 
unwisely  to  blame  solitary  causes  for  most  of  the  neuroses, 
for  other  conditioning  causes  often  conspire  with  what  we 
would  like  to  regard  as  the  prime  or  central  cause.  A 
knowledge  of  the  age  incidence  of  cancer  and  of  cases  in  the 
family,  operating  in  conjunction  with  a phase  of  depressed 
health  and  an  adverse  comment  of  a friend  upon  our  looks, 
might  surely  activate  the  imagination  in  any  one  of  us. 

Tiie  Need  for  Saner  Education 

Passing  now  to  some  general  considerations,  we  may 
observe  that  the  disease  phobias  are  on  the  whole  rarer  in  the 
simple  folk  of  the  working  classes  or  the  country-side  than 
they  are  among  the  more  sophisticated,  the  idler  well-to-do, 
the  more  educated,  and  the  office  workers.  The  spread  of 
information  to-day  is  not  all  beneficial  nor  is  it  synonymous 
with  a spread  of  knowledge.  Much  of  the  information  is 
incomplete  or  ill-digested.  Especially  is  this  so  in  the  realms 
of  human  anatomy,  physiology,  and  pathology.  Half- 
knowledge is  always  more  productive  of  fears  and  supersti- 
tions than  fuller  understanding.  More  than  one  patient  has 
consulted  me  for  an  upper  abdominal  tumour  having  for  the 
first  time  discovered  his  ensiform  cartilage! 

Anxious  parents  dread  acute  infections  and  tuberculosis 
for  their  children  and  bring  them  up  in  an  over-protected 
atmosphere,  to  their  physical  and  psychological  detriment. 
Occasionally  we  meet  with  quite  young  children  who  have 


410  OF  NOSOPHOBIA 

5.  In  the  case  of  patients  with  viscera!  or  other  symptoms 
■which  -we  believe  to  be  due  to  emotional  causes,  we  should 
explain  how  fear,  anxiety,  care,  and  worry  can  themselves 
be  the  cause  of  such  symptoms  or  at  least  serve  as  a 
contributor}’  or  perpetuating  factor. 

G.  We  are  seldom  justified  in  telling  a patient  that  * there 
is  nothing  the  matter’  but  often  in  saying  ‘there  is  no  or- 
ganic disease’.  Nor  should  we  describe  a disease  as  ‘only 
nerves’.  Such  phrases  do  not  convince  because  they  are 
both  unpopular  and  untrue.  They  express,  furthermore, 
our  own  failure  to  explain  things  to  ourselves  in  a rational 
or  physiological  way,  and  also  our  failure  to  get  behind  the 
curtain  of  our  patients*  minds. 

7.  Sometimes  in  suspected  heart  disease,  mental  disease, 
or  cancer  it  may  be  necessary  to  avoid  asking  questions 
about  the  family  history,  or  to  seek  the  information  elsewhere. 
It  cannot  help  a patient  with  anginal  symptoms  to  recall 
that  several  of  his  forebears  died  suddenly  or  a victim  of  a 
depression  to  recollect  that  on  uncle  and  a cousin  committed 
suicide. 

S.  Even  in  the  case  of  the  gravest  disease  and  even  when 
the  patient  knows  its  gravity,  much  can  be  done  to  lessen 
apprehension,  to  foster  courage  and  to  comfort  distress  by 
our  expressed  willingness  to  help  and  to  go  on  doing  all  we 
can  to  discover  the  best  means  of  help. 

0.  Kindness  and  hopefulness  are  immeasurable  assets. 
I have  not  met  such  a contradiction  in  ideas  as  a positively 
unkind  doctor,  although  I have  known  some  who  lacked 
gentleness  of  touch,  or  manner,  or  were  handicapped  by 
bad  tempers.  I have,  however,  met  some  who  were  too 
pessimistic,  or  too  silent,  who  were  careful  enough  in  their 
methods  of  examination  and  physical  treatments,  and  yet 
failed  to  meet  their  patients  with  insight  and  understanding 
and  thereby  failed  to  help  them  as  much  as  they  might  have 
done  in  their  essential  task  as  comforters. 

Looking  back  on  personal  experience  and  its  slowly 
garnered  lessons  one  is  conscious  of  many  opportunities 
lost,  of  judgements  gone  astray,  of  faults  both  of  commission 
and  omission,  but  one  is  also  conscious,  as  we  must  all  one 


XXXIII 


OBSERVATIONS  ON  THE  ABDOMINAL  AND  CIRCU- 
LATORY PHENOMENA  OF  ALLERGY1 

In  recent  times  attempts  have  been  made  to  spread  the  net 
of  allergy  too  widely.  Conditions  having  no  clinical  or 
aetiological  relationships  with  the  accepted  allergic  dis- 
orders have  been  discussed  as  possible  or  probable  examples 
of  these  disorders.  It  is  a primary  duty  of  clinical  study  to 
define  disease,  to  render  descriptions  more  precise,  and  to 
establish  diagnostic  criteria.  At  present  we  include  among 
the  allergic  disorders  asthma,  hay-fever,  spasmodic  rhinor- 
rlioea,  intermittent  hydrarthrosis,  urticaria,  angio-neurotic 
oedema,  and  eczema.  With  regard  to  migraine  and  epilepsy, 
although  they  appear  not  infrequently  in  persons  and 
families  subject  to  allergy  and  the  former  may  be  associated 
with  food  idiosyncrasies,  opinion  is  less  secure.  A paroxys- 
mal neurosis,  although  it  consorts  with  ‘nervous*  constitu- 
tions and  develops  in  response  to  minimal  stimuli,  need 
not  necessarily  depend  upon  that  type  of  idiosyncrasy 
which  allergy  implies.  Activation  of  symptoms  by  anxiety 
or  an  east  wind  would  not  at  present  be  considered  as  evi- 
dence of  allergy.  Certain  gastro-intestinal  disorders  and 
circulatory  phenomena  have  also  been  classified  as  allergic, 
but  they  stand  in  need  of  more  careful  portraiture. 

It  is  the  purpose  of  this  paper  to  identify  and  define 
certain  abdominal  syndromes  and  circulatory  disturbances 
which  may  be  reasonably  regarded  as  expressions  of  the 
allergic  state  and,  on  a purely  clinical  basis,  to  suggest 
criteria  without  which  we  should  be  unwilling  to  accept 
them  as  genuinely  allergic. 

Allergy  and  Anaphylaxis 

The  word  allergy  has  not  found  its  way  into  the  Shorter 
Oxford  Dictionary.  In  Dorland’s  Medical  Dictionary  it  is 
» Lancet,  1035,  L 1257. 


CIRCULATORY  PHENOMENA  OP  ALLERGY  413 
described  as  ‘a  condition  of  altered  susceptibility  which 
causes  an  individual  to  react  to  a second  inoculation  of 
an  antigen  in  a manner  different  from  his  reaction  to  the 
first  inoculation  (Pirquet).  The  term  is  now  used  to  denote 
the  natural  hypersensitiveness  of  an  individual  as  con- 
trasted with  anaphylaxis,  which  is  hypersensitiveness  arti- 
ficially induced  by  inoculation.  * The  clinical  relationships  of 
anaphylaxis  and  allergy  are,  however,  very  close.  Identical 
symptoms  occur  in  the  artificially  induced  and  the  spon- 
taneously developed  disorder.  Main  distinctions  between 
the  two  conditions  are  that  anaphylaxis  depends  upon  a 
specific  sensitization  and  has  a limited  course,  whereas  in 
allergic  states  precise  specificity  is  rare  or  other  forms  of 
sensitiveness  become  superimposed  upon  an  original  form, 
while  nervous  reproduction  of  symptoms  is  readily  con- 
ditioned. Cases  of  pure  horse-asthma,  for  instance,  are 
exceptional  and  in  most  asthmatics  there  is  a multiplicity 
of  circumstances  which  may  condition  or  predispose  to  the 
attack.  Furthermore,  the  clinical  course  of  an  allergic 
disorder  is  recurrent  and  unlimited. 

It  would  also  seem  that  anaphylactic  symptoms,  although 
more  readily  induced  in  persons  subject  to  allergic  disorders, 
can  be  produced  in  some  degree  independently  of  particular 
constitutional  predisposition.  Allergy,  on  the  other  hand, 
is  expressive  of  an  inborn  or  constitutional  predisposition 
and  for  this  reason  can  result  from  smaller  and  often 
infinitesimal  or  undiscoverable  stimuli. 

1 Experimental  Disease ’ in  Humans 

While  serum-sickness  is  common,  opportunities  of  study- 
ing anaphylactic  shock  in  man  are  fortunately  rare.  It  may 
baffle  observation  by  proving  immediately  fatal.  Some 
years  ago,  in  conjunction  with  J.  Fawcett,  I wrote  a paper 
entitled  ‘Cases  of  Delayed  and  Immediate  Anaphylactic 
Shock  with  a note  on  the  Circulatory  Phenomena’.1  I re- 
produce our  descriptions  and  discussion  of  two  cases  here, 
together  with  an  account  of  one  other  case  seen  since,  for 
the  sole  purpose  of  portraying  the  ‘experimental  disease’ 

* Lancet,  1023,  i.  825. 


4 U OBSERVATIONS  ON  THE  ABDOMINAL  AND 

(which  includes  both  serum-sickness  and  serum-shock),  and 
considering  thereafter  how  far  it  is  possible  to  discover 
parallel  phenomena  in  a group  of ‘spontaneous’  cases  which 
X have  since,  after  careful  consideration,  classified  in  my  files 
under  the  heading  of  allergy. 

Cask  1.  Delayed  Anaphylactic  Shock.  A young  woman,  nged  23, 
was  admitted  into  Guy’s  Hospital,  under  the  care  of  Mr.  F.  J. 
Steward,  on  5 November  1022,  with  a ‘septic’  finger.  Operations 
were  performed  on  the  6th,  8tli,  10th,  and  12th,  for  spread  of  infec- 
tion, amputation  of  the  finger  finally  becoming  necessary.  On  10  Nov- 
ember 50  c.cm.  of  ontistreptoeoccal  serum  were  given  subcutaneously 
at  the  time  of  the  operation.  Four  days  later  patches  of  urticaria  began 
to  appear,  and  there  was  slight  evening  pyrexia.  The  local  condition 
after  the  12th  progressed  satisfactorily.  At  4.30  a.m.  on  the  10th, 
8 days  after  the  scrum  was  given,  the  patient  was  wakened  by  breath- 
lessness. She  was  seen  at  5 a.m.  by  one  of  us  (J.  A.  R.)  and  was  then 
sitting  up  in  bed  with  ‘astlimatic’  breathing.  The  respiration-rate 
was  30  per  minute,  expiration  was  prolonged  and  wheezing,  and  she 
was  expectorating  small  quantities  of  clear  mucoid  sputum.  Sibilant 
expiratory  rhonchi  were  audible  all  over  the  chest.  She  was  pale,  and 
the  pulse-rate  was  between  110  and  120  per  minute.  Urticaria  was 
appearing  in  large  patches  all  over  the  trunk  and  limbs ; the  lips,  ears, 
and  eyelids  were  swollen.  The  house  surgeon,  Sir.  J.  K.  Milward, 
had  given  her  an  injection  of  liquor  adrenalin.  1-1000  2.  'Within 

20  minutes  the  asthmatic  attack  was  over,  but  she  felt  cold  and 
shivery,  the  pulse  remained  quick,  and  urticaria  continued  to  appear. 
She  was  packed  round  with  hot  blankets  and  bottles,  and  given  hot 
tea  and  lactose.  She  was  seen  again  at  8 a.m.  By  this  time  there  were 
no  asthmatic  symptoms,  but  urticaria  was  still  troublesome ; she  had 
vomited  twice,  had  two  actions  of  the  bowels,  and  was  completely 
pulseless.  She  complained  of  feeling  ‘washed  out’,  but  apart  from 
the  cutaneous  irritation  and  swelling  of  the  gums,  made  no  other 
specific  complaint;  she  was  mentally  alert,  and  quite  rational  and 
calm,  although  she  had  before  been  considerably  perturbed  by  the 
respiratory  distress.  At  10  a.m.  we  saw  her  together;  no  pulsation 
could  be  detected  at  the  wrist  or  ankle,  or  in  the  carotid  or  sub- 
clavian arteries.  The  heart  was  not  then,  or  at  any  subsequent 
observation,  perceptibly  enlarged,  and  there  were  no  murmurs.  The 
impulse  was  readily  felt,  the  rate  was  120-140  per  minute,  and  the 
sounds  were  of  good  quality.  She  was  not  cyanosed.  She  was  warm 
and  the  temperature  was  rising.  The  capillary  tide  in  the  nail-bed 
was  good.  The  question  of  further  administration  of  adrenalin  was 
discussed,  but  we  were  agreed  that,  with  such  a degree  of  tachy- 
cardia, and  no  such  urgent  indication  as  ‘asthma’  now  persisting, 
it  would  be  wiser  to  avoid  the  possible  overstress  to  the  heart  which 


CIRCULATORY  PHENOMENA  OF  ALLERGY  415 
a sudden  rise  in  blood-pressure  might  entail.  In  spite  of  her  appar- 
ently alarming  condition  a good  prognosis  was  given,  partly  on  the 
general  impression  of  the  patient’s  demeanour,  the  rising  temperature, 
and  disappearance  of  the  shiveriness  of  which  she  had  at  first  com- 
plained, and  partly 'on  the  experience  of  the  case  referred  to  below. 
For  more  than  12  hours  no  pulse  could  be  felt  at  the  wrist.  After 
24  hours  the  radial  pulse  still  could  not  be  detected  with  certainty. 
Vomiting  ceased,  but  the  patient  had  some  nausea  and  felt  that  she 
could  not  take  fluids,  except  in  the  smallest  quantities,  for  fear  that 
she  would  be  sick.  She  was  pale  and  thirsty,  had  a moist  clean 
tongue,  and  continued  to  state  that  she  felt  ‘washed  out*  and  in- 
tolerably tired,  hut  that  she  found  difficulty  in  getting  to  sleep. 

She  was  treated  throughout  with  warmth,  small  quantities  of  fluid, 
brandy  and  lactose  by  the  mouth,  and  6-hourly  rectal  administrations 
of  1 pint  of  6 per  cent,  glucose.  The  foot  of  the  bed  was  raised  for  a 
few  hours,  until  she  complained  of  the  discomfort  of  the  position. 
Sleep  was  secured  at  night  with  the  aid  of  an  opiate.  Twenty-eight 
hours  after  the  onset  of  the  attack  the  radial  pulse  could  be  felt  as  a 
doubtful  flicker,  but  not  accurately  counted.  At  the  cardiac  apex  the 
rate  could  be  readily  determined  as  120  to  130  per  minute,  but  the 
sounds  were  not  so  clear  as  on  the  previous  day.  She  now  complained 
of  acute  pain  in  nearly  all  her  joints.  She  could  not  open  her  mouth 
wide  on  account  of  pain  in  the  temporo-mandibular  joints,  and  the 
knees,  ankles,  wrists,  and  interphalangeal  joints  were  similarly  in- 
volved. There  was  no  further  trouble  with  urticaria.  Aspirin  was 
added  to  the  rectal  injections. 

Almost  abruptly  at  about  3 p.m.  on  the  19th,  or  about  34  hours 
after  the  first  appearance  of  urgent  symptoms,  the  pulse  became 
quite  good  in  volume  and  slower  in  rate,  and  from  then  onwards  It 
improved  steadily.  By  midday  on  the  20th  the  pulse-rate  was  re- 
corded as  80  per  minute.  After  a further  48  hours  all  the  joint  pains 
had  disappeared,  but  there  was  complaint  of  some  deep-seated  pain 
in  the  muscles  of  the  left  thigh.  After  this  her  progress  was  unin- 
terrupted, except  for  the  development  of  a small  patch  of  erythema 
below  the  left  knee,  and  later  of  an  abscess  in  the  right  buttock.  On 
the  morning  of  the  18th,  when  the  ‘shock’  symptoms  were  at  their 
height,  the  temperature  reached  102”,  but  quickly  fell  again  to 
normal.  It  rose  during  the  period  of  the  gluteal  abscess,  and  became 
stable  again  after  its  drainage. 

The  remarkable  feature  of  this  case  was  the  late  develop- 
ment of  severe  shock-like  symptoms,  true  anaphylactic 
shock  being  usually  considered  as  an  immediate  rather  than 
a remote  phenomenon.  Regarding  serum-sickness  as  the 
usual  anaphlyactic  response  in  human  subjects,  this  case 
might  alternatively  be  viewed  as  an  extreme  exaggeration 


410  OBSERVATIONS  ON  THE  ABDOMINAL  AND 
of  this  response,  for  the  symptoms  of  ‘serum-shock’  and 
‘serum-sickness*  were  coincident.  Indeed  the  case  suggests 
the  essential  unity  of  the  two  conditions.  The  early  develop- 
ment of  urticaria  on  the  fourth  day  was  perhaps  an  in- 
dication of  hypersensitiveness.  The  patient  was  not  an 
asthmatic  subject,  and  there  was  nothing  else  in  her  history 
to  indicate  that  she  was  previously  sensitive  to  foreign 
proteins.  She  had  at  the  time  no  recollection  of  ever  having 
had  serum  before,  but  it  was  later  elicited  from  her  mother 
tliat  she  had  had  diphtheria  nineteen  years  previously,  and 
that  she  was  given  antitoxin  at  the  time.  As  there  was  no 
history  of  alarming  symptoms  on  this  occasion  it  would 
seem  proper  to  regard  her  illness  as  a genuine  instance  of 
sensitization  by  a previous  dose.  We  thought  it  possible 
that  immediate  shock  might  have  been  averted  by  reason 
of  the  fact  that  she  was  under  an  anaesthetic  at  the  time 
of  administration  of  the  serum.  We  were  informed  by  Sir 
(then  Dr.)  P.  P.  Laidlaw  that,  although  anaesthesia  may 
relieve  or  avert  bronchial  spasm  and  so  save  life  in  the 
anaphylactic  guinea-pig,  it  has  little  effect  on  similarly  in- 
duced circulatory'  shock  in  dogs. 

Casb  2.  Immediate  anaphylactic  shock. — In  October  1018  a soldier 
was  admitted  to  a main  dressing  station  with  a small  wound  of  the 
buttock.  He  was  pale,  cold,  and  pulseless ; he  was  vomiting  and  com- 
plaining of  abdominal  pains.  So  ill  did  he  nppear  tliat  special 
examinations  were  made  to  ascertain  whether  he  might  have  an 
intra-abdominal  lesion  with  haemorrhage.  The  wound  was  carefully 
probed  and  found  to  be  quite  superficial.  He  was  not  aware  of  having 
sustained  any  other  injury.  Abdominal  examination  was  negative. 
Within  a short  while  urticaria  appeared  and  anaphylactic  shock 
could  be  confidently  diagnosed.  The  man  had  during  his  period  of 
service  received  two  previous  prophylactic  injections  of  A.T.S.,  after 
one  of  which  he  admitted  to  having  ‘felt  bad*.  He  was  examined 
probably  within  an  hour  or  less  of  receiving  the  third  dose  of  A.T.S., 
which  had  been  given  the  same  evening  at  an  advanced  dressing 
station.  Mentally  he  was  perfectly  clear.  He  was  treated  as  an  ordi- 
nary case  of  surgical  shock  by  warmth,  elevation  of  the  feet,  and 
frequent  small  sips  of  fluid,  but  as  after  2 or  3 hours  the  pulse  was 
still  Impalpable  he  was  sent  down  to  a casualty  clearing  station  with 
a special  note.  He  there  came  under  the  observation  of  Major  G.  T. 
Mullally,  who  later  reported  that  the  man  had  remained  pulseless  for 
some  hours,  but  was  fit  for  evacuation  to  the  base  on  the  follow- 


CIRCULATORY  PHENOMENA  OF  ALLERGY  417 
ing  day.  Asthmatic  symptoms  ■were  absent,  and  gastro-intestinal 
symptoms  were  the  most  prominent  apart  from  those  of  circulatory 
failure. 

The  symptoms  in  both  of  the  cases  described  suggested 
a profound  fall  in  the  systemic  blood-pressure  of  excep- 
tionally long  duration.  Presumably  the  main  volume  of 
the  blood  must  have  accumulated  in  the  splanchnic  area. 
The  absence  of  oedema  and  cyanosis,  the  rapid  recovery 
and  maintenance  of  superficial  warmth,  and  the  presence  of 
a good  capillary  tide  in  the  nail-bed  would  seem  to  exclude 
a capillary  stagnation  or  heart  failure.  There  was  no  unusual 
loss  of  fluid  by  sweating,  diarrhoea,  or  diuresis,  and  the 
fluid  intake  was  well  maintained.  The  symptoms  of  circu- 
latory shock  persisted  long  after  the  disappearance  of  the 
bronchial,  cutaneous,  and  gastro-intestinal  reactions. 

Neither  before  nor  since  have  I seen  any  other  condition 
in  which  the  state  of  pulselessness  manifest  in  these  two 
cases,  and  persisting  for  so  many  hours,  was  consistent  with 
recovery. 

Case  3.  Delayed  anaphylactic  shock. — A young  married  woman  was 
operated  on  for  acute  appendicitis  at  7 p.m.  on  17  November  1032. 
At  the  conclusion  of  the  operation  she  was  given  on  injection  of  anti- 
gas-gangrene  serum.  On  the  morning  of  Z3  November  I was  called 
urgently  to  see  her  with  Dr.  C.  H.  Atkinson.  After  a short  period  of 
malaise  she  had  abruptly  developed  acute  anaphylactic  symptoms, 
including  generalized  urticaria,  great  oedema  of  the  lips  and  eyelids, 
sensations  of  constriction  in  the  throat,  with  attendant  alarm,  pro- 
found pallor,  and  pulselessness.  An  injection  of  Jiq.  adrenalin.  1-1000 
1H.  3 was  given  immediately  and  repeated  later.  In  a few  minutes 
there  was  a rapid  improvement  and  visible  subsidence  of  the  facial 
oedema ; the  radial  pulse,  although  quick  and  small,  became  palpable ; 
the  sensation  of  constriction  departed.  Vomiting,  diarrhoea,  and 
pyrexia  followed  with  much  malaise  and  some  fever.  In  the  evening 
there  was  still  great  irritation  from  the  urticaria,  hut  the  case  gave  no 
further  anxiety.  It  ms  later  discovered  that  this  patient  had  been 
given  diphtheria  antitoxin  in  childhood  and  that  she  had  a had  rash. 
She  has  since  shown  herself  liable  to  primula  rashes. 

It  should  again  be  noted  that  this  patient  received  her 
second  dose  of  serum  while  under  an  anaesthetic.  A few 
years  ago  I had  under  my  care  a very  anaemic  patient,  who 


418  OBSERVATIONS  ON  THE  ABDOMINAL  AND 
had  twice  displayed  violent  and  alarming  immediate  ana- 
phylactic reactions  following  blood -transfusion,  but  whose 
response  to  a further  transfusion,  purposely  given  under 
anaesthesia,  passed  without  anxiety. 

On  the  experience  of  the  three  cases  described  the  circu- 
latory phenomena  of  anaphylaxis  may  be  held  to  include 
pallor,  tachycardia,  initial  coldness  of  the  surface  and  ex- 
tremities, and  pulselessness  due  to  a profound  and  sus- 
tained foil  in  blood-pressure.  In  ordinary  serum  sickness  a 
pulse-rate  of  120  per  minute  is  common.  From  the  same 
cases  we  may  also  conclude  that  vomiting,  purging,  and 
diffuse  pain  are  the  outstanding  abdominal  symptoms  of 
the  anaphylactic  state  in  man.  Asthma,  urticaria,  ‘angio- 
neurotic’ oedema,  pyrexia,  and  multiple  arthritis  are  among 
the  other  recorded  symptoms. 

Disturbances  Arising  Without  Apparent  Cause 

Let  us  now  see  how  far  these  manifestations  find  a 
parallel  (a)  in  acute  and  anxious  disturbances  arising 
spontaneously,  or  (more  correctly)  without  apparent  cause, 
and  ( b ) in  certain  chronic  or  recurring  disorders  of  less 
dramatic  character. 

Case  4.  Abdominal  allergic  attaclx;  severe  type. — A married  woman, 
aged  04,  was  brought  to  me  by  Mr.  Hastings  Gilford  on  30  December 
1931.  Except  for  malaria  many  years  previously  her  life  had  been 
healthy.  Her  daughter  suffered  from  asthma.  A year  previously  she 
had  had  an  unexplained  attack  of  malaise  and  sickness  while  abroad. 
In  November  1930  she  had  had  a sudden  severe  attack  of  epigastric 
pain  and  cholecystitis  was  suspected.  In  January  1931  she  had  an 
attack  of  quite  a different  kind,  with  violent  generalized  abdominal 
pain,  vomiting,  diarrhoea,  and  much  shock.  The  vomitus  was  slightly 
streaked  with  blood.  A succession  of  similar  attacks  followed  at 
2 to  4 weeks’  interval.  There  were  as  many  os  4 attacks  within  one 
period  of  a fortnight.  An  extreme  degree  of  shock-like  collapse 
was  evident  both  to  the  patient  and  to  others  around  her.  The  acute 
phase  was  generally  over  within  12  hours.  The  X-ray  appearances 
of  the  gall-bladder  were  normal.  She  felt  perfectly  well  between  the 
attacks.  A Chinese  spiritualist,  who  affected  to  be  able  to  see  what 
was  happening  in  the  stomach,  told  her  that  she  did  not  digest  eggsl 
Most  of  the  attacks  had  started  at  2 a.m.  In  one  of  the  attacks  her 
lips  became  tremendously  swollen  xctih  angio-neuroiic  oedema.  In  most 


CIRCULATORY  PHENOMENA  OF  ALLERGY  410 
of  them  her  tongue  ■was  raw  and  red  and  her  lips  tended  to  peel 
afterwards.  I could  find  no  signs  of  organic  disease. 

Case  5.  Abdominal  allergic  attacks;  severe  type. — A medical  man, 
aged  54,  consulted  me  for  the  attacks  to  be  described  below.  He  had 
had  malaria  and  pneumonia  in  childhood.  One  brother  had  had  hay- 
fever.  Since  childhood  he  had  been  liable  to  repeated  abdominal 
attacks  for  which  he  had  consulted  many  physicians.  His  longest  free 
period  had  been  9 months,  his  shortest  10  days.  The  attacks  generally 
started  abruptly  after  premonitory  lassitude.  Fasting  was  a predis- 
posing factor.  In  the  attacks  he  had  very  severe  generalized  ab- 
dominal pain,  starting  under  the  rib  margins,  and  of  crescendo  type. 
Nausea  sometimes  preceded,  sometimes  succeeded  the  onset  of  pain. 
Vomiting  followed,  and  if  it  came  early  the  attack  passed  more  quick- 
ly. He  was  unable  to  eat  or  drink  during  the  attacks,  which  would 
last  from  24  to  48  hours.  Throughout  the  attack  he  looked  extremely 
pale  and  ill,  and  the  pulse-rate  rose  to  120.  He  had  a slight  inguinal 
hernia,  and  during  the  attack  • the  sac  seemed  to  fill  with  fluid’,  which 
he  could  press  back  into  the  abdomen.  The  abdomen  was  slightly 
swollen  and  it  hurt  him  to  take  a deep  breath.  He  had  given  up  pork 
and  bacon  because  one  attack  followed  a pork  pie,  and  mushrooms 
and  fish  because  his  skin  had  shown  a slight  reaction  to  these,  but 
without  benefit.  In  one  attack  a surgeon  was  called  to  see  if  he  had 
appendicitis.  Between  the  attacks  he  felt  perfectly  well.  He  had 
had  hay-fever  for  80  years,  and  for  12  years  at  intervals  he  had  been 
subject  to  angio-neurotic  oedema  of  his  hand,  arm,  and  perineum,  and 
on  five  occasions  of  the  palate  and  uvula,  for  which  he  had  entered 
a nursing-home,  fearing  that  trachcotomj'  might  become  necessary. 
Excepting  for  a right  inguinal  hernia  and  a myotoni c right  pupil,  first 
noticed  80  years  previously,  there  were  no  signs  of  any  organic  disease. 

In  both  of  these  cases  we  find  gastro-intestinal  and 
circulatory  phenomena  closely  comparable  with  those  shown 
by  the  patients  with  anaphylaxis,  and  including  shock, 
pallor,  tachycardia,  vomiting,  diarrhoea,  and  abdominal 
pain.  In  addition  we  have,  as  confirmatory  evidence,  simul- 
taneous or  associated  angio-neurotic  oedema  in  both  cases, 
hay-fever  in  one,  and  a solitary  relative  with  an  allergic 
disorder  in  both  cases. 

Before  reviewing  the  less  dramatic  hut  more  frequent 
allergic  dyspepsias  (in  which  circulatory  manifestations  are 
lacking  or  inconspicuous)  there  are  further  points  in  con- 
nexion with  the  vasomotor  phenomena  of  anaphylaxis  and 
allergy  which  will  bear  consideration.  Together  with  the 
objective  pulse  and  blood-pressure  disturbances  of  acute 


420  OBSERVATIONS  ON  THE  ABDOMINAL  AND 
anaphylaxis  from  scrum  there  may  be  associated  the  ‘sense 
of  impending  death’  which,  in  conjunction  with  striking 
vasomotor  symptoms,  is  so  pronounced  a feature  of  vaso- 
vagal attacks  (Gowers’s  syndrome).  Vasovagal  attacks 
chiefly  affect  patients  who  are  at  the  same  time  physically 
unfit  and  in  a state  of  anxiety.  There  is  also,  however,  an 
occasional  association  between  vasovagal  attacks  and  mi- 
graine, nsthma,  epilepsy,  spastic  colon,  and  angio-neurotic 
oedema.  All  in  fact  proclaim  an  inborn  hypersensitiveness 
which  may  be  expressed  in  one  or  more  of  these  several 
ways.  It  is  rare  in  any  of  these  to  discover  a specific 
sensitiveness  as  a basis  for  the  vasovagal  episodes,  but  an 
occasional  case  may  develop  symptoms  in  the  first  instance 
in  response  to  a specific  cause. 

Cash  C.  Vasovagal  attacks  following  a second  dose  of  serum. — A 
young  man,  aged  21  (a  patient  of  Dr.  A.  IV.  Walters),  whose  feeding 
in  infancy  Imd  caused  much  trouble  and  who  had  suffered  from 
‘mucous  disease’  until  the  age  of  7,  was  thereafter  fairly  healthy 
until  the  age  of  18.  He  then  sustained  a concussion  and  fractured 
a leg  in  a motor-cycle  accident,  and  was  given  tetanus  antitoxin.  At 
the  age  of  21  he  was  involved  in  another  motor-cycle  accident,  was 
again  concussed,  and  fractured  a small  bone  in  his  left  hand,  and  was 
again  given  antitoxin.  After  this  he  was  very  unfit  with  urticaria 
nnd  pyrexia,  and  developed  attacks  in  which  he  was  suddenly  seized 
with  a feeling  of  impending  death  and  uncomfortable  sensations  about 
his  heart.  These  attacks  would  last  from  1 to  1 hour.  "When  he 
sought  to  change  his  position  things  seemed  to  ‘black  out’  and  he 
felt  ‘wobbly’  at  the  knees.  He  was  terribly  scared  by  these  attacks, 
notwithstanding  that  he  knew  little  of  physical  fear,  was  a keen  rider 
to  hounds,  a member  of  the  Auxiliary  Air  Force,  and,  as  his  history 
suggests,  a none  too  cautious  motor-cyclist. 

The  attacks  continued  for  a time  otter  the  phase  of  serum-sickness. 
His  father  had  experienced  similar  attacks  at  the  age  of  27  but  had 
outgrown  them.  I have  no  notes  as  to  his  appearance  during  these 
attacks  but  the  subjective  phenomena  were  those  of  Gowers’s  syn- 
drome, of  which  the  usual  objective  manifestations  are  pallor,  cold- 
ness, and  striking  pulse  and  blood-pressure  fluctuations.  Had  he 
experienced  a solitary  attack  with  urticaria  immediately*  after  the 
serum  we  should  have  accepted  It  as  typical  of  anaphylaxis.  It  is 
reasonable  to  argue  that  the  succession  of  attacks  in  this  instance  was 
initiated  by  a second  dose  of  serum.  The  infantile  and  family*  histories 
suggest  the  conjunction  with  the  therapeutic  ‘experiment’  of  an 
appropriate  ‘constitution’. 


CIRCULATORY  PHENOMENA  OP  ALLERGY 


421 


Allergic  Dyspepsias 

It  is  not  uncommon  to  meet  persons  who  are  aware  of 
a food-idiosyncrasy.  Shell-fish  and  eggs,  especially  ducks’ 
eggs,  are  well-known  offenders  and  may  give  rise  to  gastric 
disturbances  and  erythematous  or  urticarial  rashes.  More 
rarely  chocolate  or  coffee  is  blamed.  Idiosyncrasies  for 
drugs,  not  excluding  those  in  common  use  like  morphine 
(which  may  cause  vomiting  and  collapse),  are  well  recog- 
nized. The  victims  of  these  idiosyncrasies,  however, 
although  (like  the  horse-asthmatic)  they  exemplify  a specific 
sensitiveness,  usually  have  the  sense  to  avoid  what  is 
poisonous  to  them  and  are  rather  less  likely  to  consult 
us  for  recurring  allergic  disturbances  than  those  whose 
sensitiveness  lacks  discoverable  specificity.  Of  this  latter 
group,  I have  selected  a few  examples  from  my  files.  The 
case  histories  illustrate  some  of  the  types  of  gastric  and 
colonic  disturbance  which  may  be  encountered  and  my 
reasons  for  regarding  them  as  allergic. 

Case  7. — A medical  man,  aged  59,  developed  indigestion  at  a time 
of  great  strain.  A suspicion  of  duodenal  ulcer  was  entertained  but  not 
confirmed.  At  the  same  time  he  developed  angio-neurotic  oedema 
affecting  the  lips  and  eyelids  particularly,  and  developing  usually  on 
waking  in  the  morning.  Wien  he  went  on  holiday  he  lost  both  the 
dyspepsia  and  the  angio-neurotic  oedema.  Later,  with  an  access  of 
work  and  worry,  the  symptoms  recurred  and  the  scrotum  and  penis 
also  became  affected  by  the  oedema.  At  this  time  he  did  not  lose  the 
symptoms  on  a holiday.  His  father  had  hay-fever.  Two  sisters  and 
too  brothers  had  asthma.  One  sister  had  chronic  urticaria.  II is  daughter 
was  asthmatic.  His  dyspeptic  symptoms  developed  between  2 and 
3 hours  after  food,  and  he  sometimes  had  hunger-pain  in  the  night. 
He  was  Bleeping  badly  and  was  very  tired  when  I saw  him. 

I found  no  signs  of  organic  disease,  and  prescribed  a third  partner, 
tnedinal  at  bedtime,  and  an  early  retirement  from  practice. 

He  wrote  to  me  8 months  later  as  follows:  ‘You  will  be  interested 
to  hear  that  since  I have  had  better  nights  my  digestive  apparatus 
lias  been  quite  a different  thing,  and  I have  had  no  signs  of  the  giant 
urticaria  which  troubled  me  last  winter.’  Now,  2 years  later,  he  has 
retired  from  practice  and  remains  perfectly  well. 

Non-specific  treatment,  as  with  asthma,  may  sometimes 
play  a useful  part  in  ‘uncondi  turning’  allergic  symptoms. 


422  OBSERVATIONS  ON  THE  ABDOMINAL  AND 

Case  8.  A young  woman,  aged  32,  was  brought  to  me  by  Dr.  C. 
Boyson  on  account  of  a series  of  attacks  of  abdominal  pain  in  the 
course  of  the  descending  colon,  lasting  perhaps  20  minutes.  Six  weeks 
and  2 years  previously  she  had  had  bad  attacks  of  pain  in  which  she 
was  ‘doubled  up*.  For  over  ten  years  she  liad  been  worried  by  inde- 
finite abdominal  pains,  and  both  the  gall-bladder  and  the  appendix 
had  come  under  suspicion.  At  times  she  had  feelings  of  extreme 
emptiness.  She  was  of  nervous  type.  She  believed  that  influenza 
could  precipitate  an  abdominal  attack,  and  that  worries  and  smoking 
aggravated.  The  gall-bladder  was  radiologically  normal.  There  was 
indefinite  tenderness  in  the  right  iliac  fossa.  In  childhood  and  later 
she  had  been  troubled  with  eczema,  and  throughout  adult  life  by  hay- 
fever  and  a spasmodic  rhinorrhoea  which  was  induced  by  proximity 
to  horses.  One  brother  was  asthmatic  and  her  father  was  a 'sneezer'. 
Later  she  was  seen  in  an  attack  of  cholecystitis  with  slight  icterus  and 
local  tenderness  over  the  gall-bladder. 

Case  0.  A retired  mining  engineer,  aged  70  (referred  by  Dr.  D.  R. 
Pike),  had  suffered  from  heartburn  for  many  years  with  aggravation 
latterly.  He  was  chiefly  troubled  between  3 and  0 ami.,  when  he  was 
wakened  by  oesophageal  burning  and  spasm,  choking  and  hiccups, 
and  would  expectorate  much  watery  fluid.  A diagnosis  of  duodenal 
ulcer  had  been  made  by  one  physician,  although  there  was  no  radio- 
logical confirmation.  He  was  intolerant  of  salt  meat  and  Vermouth, 
and  knew  his  evening  cigar  ‘did  him  no  good’.  His  mother  and 
maternal  uncles  had  asthma.  He  himself  Ehowed  a well-marked 
factitious  urticaria. 

Case  10,  A married  woman,  aged  37,  a patient  of  Dr.  F.  G.  France, 
gave  a long  history  of  abdominal  pain,  had  seen  many  physicians,  and 
been  fully  investigated  in  a London  hospital,  without  result  or  benefit. 
Seven  years  previously  she  had  had  a hysterectomy  for  menorrhagia 
and  dysmenorrhoea.  Her  complaint  was  of  a dull,  aching,  linear  pain 
in  the  course  of  the  descending  colon,  with  aggravation  by  worry, 
exertion,  and  after  defaecation,  features  characteristic  of  the  ‘spastic 
colon’.  The  stools  were  rather  loose,  and  she  had  a feeling  that  the 
bowel  was  never  empty.  Apart  from  a myotonic  left  pupil  there  was 
no  evidence  of  organic  disease.  She  also  suffered  from  urticaria  and 
hay-fever,  and  her  mother  had  suffered  from  urticaria. 

Case  11.  A married  woman,  aged  38,  with  three  young  children, 
was  brought  to  see  me,  by  Dr.  It.  IV.  Todd,  for  recurring  abdominal 
crises  characterized  by  severe  abdominal  pain,  profuse  vomiting,  even 
water  being  rejected,  a temperature  not  exceeding  00°,  and  a quick 
pulse.  There  was  general  tenderness  in  the  attacks  with  ‘serai- 
rigidity’,  but  no  distension.  Appendicitis  had  been  queried.  In  one 
attack  the  pain  was  chiefly  epigastric ; in  another  right-sided.  Mor- 
phine had  been  given  on  one  occasion.  The  attacks  passed  over  in  2 


CIRCULATORY  PHENOMENA  OF  ALLERGY  423 
or  3 days.  After  her  last  pregnane}’,  a year  previously,  the  bowels  had 
been  slightly  loose.  One  attack  had  followed  shell-fish.  She  had  also 
had  slight  attacks  of  angio-ncurolic  oedema  affecting  the  lip  and,  fol- 
lowing the  last  abdominal  seizure,  some  ‘large  raised  bumps’  on  the 
back  of  the  neck.  She  had  always  been  liable  to  ‘acidity’  and  skin 
troubles.  In  her  most  recent  attack  there  was  headache.  On  several 
occasions  she  had  experienced  extremely  severe  attacks  of  rectal 
spasm  lasting  20  minutes.  Her  first  baby  suffered  from  universal 
eczema.  Apart  from  slight  deep  tenderness  in  the  right  iliac  fossa 
there  was  no  evidence  of  disease. 

One  of  the  chief  difficulties  in  cases  of  this  type  is  the 
differentiation  from  appendicitis.  It  is  also  to  be  remem- 
bered that  appendicular  infection  or  a gall-bladder  infection 
may  (as  I have  more  than  once  been  led  to  believe)  act  as 
the  ‘sensitizer'  in  a patient  with  allergic  tendencies.  Dia- 
gnostic finality  in  cases  of  this  kind  may  only  be  attained 
by  a ‘follow  up’  over  a period  of  years.  The  association  of 
cutaneous  or  other  allergic  phenomena  with  abdominal 
attacks  can  never  of  itself  exclude  a more  organic  basis  for 
such  attacks. 

Case  12.  A married  woman,  aged  50,  highly  strung  and  fond  of 
good  living  (seen  with  Dr.  C.  II.  Atkinson),  had  shown  unusually 
severe  reactions  to  the  extraction  of  teeth  and  also  to  vaccines  pre- 
pared from  them  as  a treatment  for  rheumatism.  Over  a period  of 
2 or  8 years  she  had  several  extremely  severe  abdominal  attacks, 
starting  with  a girdle-like  pain  of  colicky  character,  which  at  times 
‘doubled  her  up*  and  necessitated  morphine.  With  some  of  them  she 
experienced  headache.  A year  priOT  to  my  being  called  to  see  her  she 
had  been  troubled  by  a very  obstinate  urticaria,  which  eventually 
departed  after  calcium  injections.  On  12  April  1034  she  felt  ‘off 
colour*,  nervy  and  irritable,  and  then  had  one  of  these  attacks  with 
passage  of  pale  stools,  atemperature  of  101-4,  and  a pulse-rate  of  100. 
This  attack,  like  the  others,  passed  off  ‘in  a day  or  two’.  Possible 
precipitating  causes  had  been  shell-fish,  smoked  salmon,  and  cream. 
She  was  intolerant  of  eggs  and  chocolate.  As  a child  she  had  had 
bronchial  troubles.  Her  doctor  had  seen  her  with  spasmodic  pain  In 
the  descending  colon.  I saw  her  on  13  April  and  could  find  no  signs 
of  organic  disease,  and  was  of  the  opinion  that  her  pains  were  colonic 
and,  perhaps,  an  expression  of  allergy.  On  5 June  1934  she  had  a 
very  bad  attack  of  upper  abdominal  pain  without  vomiting  j tempera- 
ture SO9.  There  was  some  tenderness  In  the  right  iliac  fossa.  She  was 
operated  on  that  night  for  appendicitis  (retro-caeeal)  with  localized 
peritonitis.  After  her  wound  had  healed  she  experienced  further 
trouble  with  obscure  temperatures  and  abdominal  pains. 


424  OBSERVATIONS  ON  THE  ABDCNHNAL  AND 
Summary 

Cases  of  ‘spontaneous’  sensitization  or  allergy  have  been 
compared  with  cases  of  ‘ experimental’  sensitization  or  ana- 
phylaxis. There  is  a close  parallelism  between  the  symptoma- 
tologies, subjective  and  objective,  of  serum-anaphylaxis 
and  certain  rare  and  alarming  seizures  occurring  with- 
out apparent  cause.  These  seizures  are  characterized  by 
simultaneous  gastro-intestina!  and  circulatory  symptoms, 
together  with  cutaneous  manifestations  or  an  associated 
history  of  these.  They  affect  persons  with  individual  and 
familial  liabilities  to  astlima,  hay-fever,  and  urticaria.  In 
other  persons  showing  similar  liabilities  we  also  discover  a 
tendency  to  chronic  or  recurring  disorders  of  stomach  and 
bowel. 

Generalized  abdominal  pain,  vomiting,  and  diarrhoea,  on 
the  one  hand,  and  pallor,  tachycardia,  and  other  shock-like 
manifestations  on  the  other,  are  the  features  of  the  more 
severe  and  acute  disorder.  In  one  case  I have  seen  severe 
recurrent  bleeding  from  the  bowel  akin  to  that  described 
by  Dean  and  Webb  in  experimental  anaphylaxis  in  dogs.1 
Recurring  pain,  of  less  intense  type,  in  the  gullet,  stomach, 
and  bowel,  sometimes  simulating  organic  disease,  and  loose- 
ness of  the  bowels  are  the  main  features  of  the  more  chronic 
dyspepsias. 

There  is  little  to  distinguish  the  circulatory  phenomena 
and  subjective  sensations  of  some  vasovagal  attacks 
{Gowcrs’s  syndrome)  from  those  of  anaphylactic  shock,  and 
cases  of  Gowers’s  syndrome  may  create,  at  the  time  of  the 
attack,  an  equivalent  degree  of  alarm.  A case  of  Gowers’s 
syndrome  following  a second  inoculation  of  tetanus  anti- 
toxin is  described. 

Referring  to  my  notes  of  nineteen  cases  filed  under  the 
heading  of  angio-neurotic  oedema,  I find,  in  addition  to 
Case  7,  two  examples  of  associated  dyspeptic  disturbance 
and  two  of  associated  vasovagal  attacks.  A similar  inquiry 
by  cross-reference  into  my  much  larger  asthmatic  series 

1 Dean,  H.  R.,  and  Webb,  R.  A.,  Joum.  of  Path,  and  Bad.,  1024, 
xxvil.  SI. 


CIRCULATORY  PHEN03EENA  OF  ALLERGY  425 
would  necessitate  a more  laborious  inquiry,  but  the  associa- 
tion of  asthma  with  digestive  and  other  allergic  disorders  is 
well  recognized . With  relapsing  and  evanescent  disturbances 
such  as  those  under  review  we  depend,  of  necessity,  for 
advances  in  our  knowledge  more  upon  detailed  clinical 
observations  and  case  histories  than  upon  any  other  method 
of  approach.  The  therapeutics  of  the  individual  case  are 
also  better  served  by  close  clinical  scrutiny  and  adjustments 
based  thereon  than  by  allegiance  to  a particular  method. 

Conclusions 

No  abdominal  or  circulatory  disturbance  should  be 
labelled  as  ‘allergic’  unless  two  or  preferably  more  of  the 
following  postulates  are  fulfilled: 

(1)  The  symptoms  should  bear  close  comparison  with 
those  observed  in  human  anaphylaxis  or  serum-sickness. 

(2)  There  should  be  a history  of  idiosyncrasy  in  respect 
of  some  food,  beverage,  tobacco,  drug,  or  other  extraneous 
substance. 

(8)  There  should  be  observed,  either  in  conjunction  or 
alternating  with  the  abdominal  or  circulatory  episodes, 
other  accepted  allergic  phenomena  such  as  asthma,  hay- 
fever,  urticaria,  or  angio-neurotic  oedema. 

(4)  There  should  be  a family  history  of  these  disorders. 

(5)  The  disturbances  should  show  some  such  intermit- 
tency  or  periodicity  as  obtains  with  other  allergic  disorders. 

(6)  Every  care  should  have  been  taken  to  exclude  organic 
disease. 

To  these  A.  F.  Hurst1  would  add  the  occurrence  of  eosino- 
philia  and  a favourable  response  to  the  therapeutic  admini- 
stration of  adrenalin  during  attacks.  My  cases  have  all  been 
seen  in  the  course  of  consultative  work,  and  I have  had  few 
opportunities  of  putting  these  additional  tests  to  the  proof. 

* In  Price’s  Text-hook  of  the  Practice  of  Medicine,  London,  1033. 


xxxrv 

DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN 

In  the  year  2S8i  Jonathan  Hutchinson  published  a series  of 
six  lectures  on  ‘Temperament,  Idiosyncrasy  and  Diathesis’, 
suitably  entitling  his  book  The  Pedigree  of  Disease  and 
dedicating  it  to  the  memory  of  Charles  Darwin.  His  opening 
lecture  includes  the  following  sentences: 

' Our  forefathers,  who  knew  far  less  about  the  details  of  pathology 
than  we  do,  attached  far  more  importance  to  such  matters  as  tem- 
perament and  diathesis.  They  were  accustomed  to  prescribe  for  a 
man’s  temperament ; we  think  only  of  his  disease,  and  turn  aside  with 
weariness  from  classifications  of  diathesis  in  which  the  physicians  of 
an  older  day  delighted.  Although  to  a large  extent  this  change  of 
sentiment  has  been  the  result  of  advance  in  knowledge,  yet  I think 
it  might  easily  be  shown  that  it  has  gone  too  far,  and  that  we  now 
neglect  unwisely  the  study  of  those  differences  between  man  and  man 
of  which,  for  the  most  part,  physiology  takes  no  cognizance,  but  which 
may  yet  prove  of  much  importance  in  modifying  the  processes  of 
disease.’ 

Ten  years  ago  these  words  could  have  been  rewritten 
with  equal  truth,  for  the  whole  subject  of  constitution  as  a 
factor  in  morbidity  had  continued  to  suffer  a curious  neglect 
at  the  hands  of  our  profession.  This  neglect  was  in  part  due 
to  the  birth  and  growth  of  bacteriology,  with  its  concen- 
tration on  the  extraneous  causes  of  disease,  and  in  part  also 
to  the  perfection  of  biochemical  and  histological  methods 
and  a preoccupation  ■with  the  intimate  processes  and  effects 
of  disease  which  these  in  turn  engendered.  It  is  true  that 
physicians  have  never  omitted  to  place  a certain  reliance 
upon  family  histories,  and  that  the  genetics  of  a few  rare 
maladies  have  been  carefully  and  profitably  studied.  Until 
recency,  however,  there  was  iVttfe  direct  inquiry  info  the 
problems  of  constitutional  predisposition  and  immunity. 
Indeed  the  whole  doctrine  of  diatheses  was  by  some  sub- 
jected to  a measure  of  ridicule  which  a closer  attention  to 
the  teachings  of  Darwin  and  his  disciples  might  at  any  time 
have  discountenanced. 


DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN  427 
In  the  last  few  years  Draper  in  the  United  States,  and  in 
this  country  Garrod,  Hurst,  Rolleston,  Langdon  Brown,  and 
the  •writer  of  the  present  paper  have  endeavoured  to  revive 
interest  in  the  study  of  ‘those  differences  between  man  and 
man 1 which  are  associated  with,  or  concerned  in  maintaining 
a liability  to  or  freedom  from,  some  common  forms  of  disease. 
Medicine  owes  much  to  genetics  and  genetics  owe  not  a 
little  to  medicine.  In  the  future  we  shall  look  to  a closer 
co-operation  between  geneticists  on  the  one  hand  and 
students  of  human  physiology  and  pathology  on  the  other. 
From  the  physiologists  in  particular  may  we  not  expect  a 
better  attention  to  the  problems  of  individual  physiology 
and  a clearer  recognition  of  the  fact  that  for  no  particular 
structure  or  function  is  it  possible  to  establish  an  absolute 
standard  of  normality  ? Although  the  variations  about  the 
mean  may  be  slight  indeed  they  are  sometimes  of  the 
greatest  importance  in  that  they  serve  to  shape  the  destiny 
of  the  individual,  for  better  or  for  worse,  in  his  conflicts  with 
natural  adversity. 

Morbid  characters  are  transmissible  from  one  generation 
to  another  in  accordance  with  the  same  laws  as  those  affect- 
ing the  transmission  of  favourable  or  neutral  characters. 
They  may  be  conveniently  subdivided  into:  (I)  morbid 
structures,  (2)  morbid  functions,  and  (3)  morbid  disposi- 
tions. Between  these  the  differences  are,  perhaps,  more 
apparent  than  real,  for  inherited  morbid  functions,  such  as 
colour-blindness  and  haemophilia,  probably  depend  upon 
minute  differences  of  cellular  or  molecular  structure,  and  a 
morbid  disposition  or  diathesis  may  be  said  to  represent  a 
liability  to  unusual  or  variable  function  or  reaction  in  the 
presence  of  environmental  stress. 

Hare-lip,  supernumerary  digits,  and  achondroplasia  are 
examples  of  heritable  structural  defect.  Colour-blindness 
and  haemophilia  have  already  been  cited  as  examples  of 
inherited  physiological  flaw.  All  of  these  are  present  at 
birth,  and,  unless  they  be  surgically  corrigible,  persist 
through  life.  Morbid  dispositions  include  those  peculiarities 
of  tissue  or  tissue-response  which  carry  with  them  in  a 
subject  healthy  at  birth  and  sometimes  throughout  life 


428  DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN 
n low  immunity  to  the  tubercle  bacillus  or  other  bacteria, 
or  a liability,  especially  in  adult  life  and  in  the  presence  of 
certain  habitual  or  environmental  influences,  to  such  chronic 
or  relapsing  diseases  as  gout,  asthma,  migraine,  epilepsy, 
hyperpiesia,  duodenal  ulcer,  and  pernicious  anaemia.  Here 
we  are  only  concerned  with  the  morbid  dispositions  or 
diatheses.  Before  discussing  these  in  closer  detail  certain 
definitions  of  terms  reclaimed  for  proper  usage  are  desirable. 

Constitution  and  Diathesis 

By  the  term  constitution  should  be  understood  the  sum* 
total  of  inborn  qualities,  anatomical,  physiological,  psycho- 
logical, and  immunological,  of  which  the  individual  is 
compounded,  or  his  whole  endowment  from  the  parental 
germ-plasm.  By  a constitutional  disease  we  should  therefore 
imply  not  a general  as  opposed  to  a local  disease,  but  one 
dependent  upon  peculiarities  of  constitution  or  the  qualities 
of  the  germ-plasm. 

Diathesis  is  described  in  Borland's  Medical  Dictionary  as 
* a natural  or  congenital  predisposition  to  a special  disease*. 
Hutchinson  [I]  defined  diathesis  as  ‘any  condition  of  pro- 
longed peculiarity  of  health  giving  proclivity  to  definite 
forms  of  disease*.  In  naming  a particular  diathesis  we 
should  couple  the  term  with  the  disease  to  which  the 
predisposition  exists,  such  as  the  ‘gouty  diathesis',  and  not 
with  the  constitutional  peculiarities  which  are  found  in 
association  with  it.  Hurst  [2],  in  describing  the  physical 
characteristics  encountered  in  association  with  duodenal 
ulcer,  has  used  the  term  ‘hypersthenic  gastric  diathesis*. 
It  would  be  more  correct  to  speak  of  the  ‘ulcer  diathesis’ 
and  to  state  that  it  occurs  in  company  with,  or  as  a part  of, 
the  ‘hypersthenic  constitution*. 

To  maintain  conformity  with  biological  concepts  I have 
suggested  that  a diathesis  should  be  considered  as  ‘a  varia- 
tion in  the  structure  or  function  of  tissues  which  renders 
them  peculiarly  liable  to  react  in  a certain  way  to  certain 
extrinsic  stimuli’.  Sir  Archibald  Garrod  [3]  has  been  kind 
enough  to  give  this  definition  his  blessing  in  his  recent 
monograph  on  inborn  factors  in  disease. 


DIATHESIS  OR  VARIATION  AND  DISEASE  IN  MAN  429 


Variation 

We  owe  to  Darwin  the  important  conception  of  variation, 
for  lie  showed  that  although,  in  the  main,  like  begets  like, 
there  is  also  a constant  tendency  among  species  to  vary  in  a 
greater  or  less  degree  and  that  under  conditions  of  domes- 
ticity variability  in  animals  is  greatly  increased.  Naturalists 
have  studied  extensively  the  variability  of  wild  forms,  but 
this  is  generally  slight  as  compared  with  the  variability 
occurring,  for  instance,  among  dogs  and  domestic  pigeons. 
There  is,  as  Huxley  [4]  indicated,  no  real  difficulty  about 
the  fact  of  variability  inasmuch  as  the  organism  propagated 
proceeds  from  two  stocks  with  different  qualities  and  prepo- 
tencies and  ‘cannot  be  an  exact  diagonal  of  the  two’.  The 
human  race  also  shows  wide  variations,  and  in  a nation  or 
even  in  a single  family  we  still  find  very  perceptible  and 
distinctive  variations  in  respect  of  colour,  stature,  tempera- 
ment, stamina,  ability,  and  longevity.  These  are  in  large 
part  germinal,  and  in  common  with  all  true  variations  are 
transmissible  from  one  generation  to  another.  Is  it  sur- 
prising that  we  should  find  comparable  variations  in  respect 
of  liability  or  resistance  to  disease  ? 

If  a diathesis  be  regarded  as  a biological  variation  and, 
like  all  true  variations,  transmissible,  it  at  once  becomes 
comparable  with  such  favourable  variations  as  pave  the 
way  to  longevity,  athleticism,  and  high  intellectual  attain- 
ment. Further,  it  is  only  reasonable  to  argue  the  existence 
of  unfavourable  as  well  as  of  neutral  or  favourable  varia- 
tions. It  could  scarcely  be  otherwise.  Above  and  below  the 
mean  or  average  and  most  convenient  stature  there  must 
be,  within  certain  limits,  every  conceivable  variation  of 
stature.  And  above  or  below  the  mean  or  average  resistance 
to  tuberculosis,  or  power  to  metabolize  or  excrete  uric  acid, 
there  must,  within  limits,  be  every  conceivable  quantitative 
variation.  At  the  extremes  we  meet  with  peculiar  resistance 
or  susceptibility  to  the  disease  in  question.  The  case  for 
diathesis  may  be  put  more  tersely  by  saying  that  the  more 
abnormal  a man  is  within  the  limits  of  health  and  in  respect 
of  certain  qualities,  the  more  readily  will  he,  in  appropriate 


430  DIATHESIS,  OR  VARIATION’  AND  DISEASE  IN  MAN 
circumstances,  be  precipitated  into  a particular  state  of 
ill  health. 

It  must  be  clearly  appreciated  that  constitution  and 
diathesis  arc  not  interchangeable  terms.  Rather  is  the  dia- 
thesis a part  or  a feature  of  the  constitution.  Physicians 
through  the  ages  have  recognized  an  association  between 
certain  diseases  and  certain  types  of  physique  or  tempera- 
ment or  certain  peculiarities  of  texture  or  colouring.  These 
traits  ore  also  a part  or  feature  of  the  constitution.  Their 
presence  may  help  to  the  recognition  of  a diathesis,  but  for 
the  most  part  they  do  not  explain  it.  Thus  dark-haired, 
dark-complexioned  people  are  more  liable  to  constipation 
and  abdominal  disorders,  and  blue  or  grey-eyed  subjects 
to  the  skin  disease,  psoriasis,  but  the  dark  hair  and  the  blue 
eyes  do  not  in  any  way  explain  these  proclivities. 

For  a disease  to  be  classified  as  constitutional,  I would 
suggest  that  one  or  more  of  the  following  postulates  arc 
necessary:  (1)  a clear  family  history  of  the  disease  should  be 
frequently  obtained ; (2)  there  should  be  frequently  asso- 
ciated with  itnotable  physical,  physiological,  orpsychologtcal 
peculiarities  (i.e.  correlated  variations) ; (3)  some  peculiarity’ 
of  structure  or  function  present  in  health  and  capable  of 
explaining  the  predisposition  should  be  demonstrable. 

I have  elsewhere  [5]  discussed  some  of  the  arguments  in 
favour  of  a constitutional  factor  in  diseases  as  diverse  as 
tuberculosis,  rheumatic  fever,  scarlet  fever,  diphtheria,  duo- 
denal ulcer,  ‘visceroptosis’,  hyperpiesia,  angina  pectoris, 
gout,  asthma,  migraine,  epilepsy,  and  pernicious  anaemia. 
In  relation  to  some  diseases  we  recognize  at  present  only 
the  fact  of  greater  or  less  immunity  or  predisposition  in 
certain  families  or  races.  In  relation  to  others  we  recognize 
a definite  tendency  for  the  predisposition  to  be  passed  on 
immediately  through  the  generations.  In  relation  to  others, 
again,  we  may  add  the  occurrence  of  correlated  variations 
in  the  shape  of  peculiarities  of  colouring,  physique,  or  tem- 
perament. Finally  in  a few  we  can  go  farther  still  and  put 
a finger  on  the  actual  anatomical  or  physiological  variant 
w’hich  seems  to  explain,  at  least  in  part,  the  particular 
predisposition. 


DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN  431 

I propose  to  confine  myself  to  two  diseases,  already 
reviewed  in  some  of  these  connexions  by  Hurst  [2],  in  which 
we  may,  employing  our  three  postulates,  recognize  simul- 
taneously the  occurrence  of  positive  family  histories,  of 
correlated  variations,  and  of  a peculiarity  of  function, 
discoverable  both  in  patients  and  in  the  course  of  an  inves- 
tigation of  healthy  subjects,  which  appears  to  provide  a 
reasonable,  if  partial,  explanation  of  the  actual  proclivity. 

The  Ulcer  Diathesis 

In  1921  Izod  Bennett  [6]  and  I performed  fractional 
gastric  analyses  on  one  hundred  healthy  male  medical 
students.  The  extremes  of  variability  in  their  curves  of 
gastric  acidity  are  shown  in  the  accompanying  chart. 
Eighty  per  cent,  of  the  total  were  found  to  give  curves 
falling  within  the  limits  indicated  by  the  transverse  hatch- 
ing, and  this  zone  has  been  adopted  as  the  ‘normal’  stan- 
dard for  test-meal  charts  in  clinical  use.  Eight  healthy 
subjects  gave  curves  of  acidity  which,  on  previous  ex- 
perience, would  have  been  regarded  as  pathologically  high, 
and  of  these  five  were  of  the  ‘climbing’  hyperclilorhydric 
type  which  we  now  associate  with  duodenal  ulcer. 

Now  the  hyperchlorhydria  of  duodenal  ulcer  is  not  only 
present  in  the  great  majority  of  cases  (70-80  per  cent.), 
but  is  also  constant  in  the  individual  and  persists  at  all 
times  whether  the  ulcer  be  active  or  quiescent.  Experimen- 
tally in  animals  ulcers  are  perpetuated  by  an  artificial 
hyperchlorhydria  (Bolton).  The  suggestion  that  hyper- 
chlorhydria, occurring  as  an  inborn  variation,  is  a predis- 
posing factor  to  the  birth,  or  at  any  rate  to  the  perpetuation, 
of  a duodenal  ulcer  becomes  therefore  a very  reasonable 
hypothesis.  But  let  us  inquire  into  the  other  evidence  for  a 
constitutional  factor  in  duodenal  ulcer.  First,  in  respect  of 
family  history,  we  obtain  in  at  least  10  per  cent,  of  all  eases 
an  account  of  one  or  more  proved  cases  of  duodenal  ulcer 
in  near  relatives  [7].  In  one  case  of  mine  the  father  of  the 
patient,  two  uncles,  and  a cousin ; in  another  three  brothers ; 
in  a third  a sister  and  two  maternal  cousins  had  been 
afflicted.  In  a fourth  family  both  parents,  three  sons,  one 


IIHHHII 


■■K  EKBB9  1 

iinflHBBiinnin 


WA&vmm 


Variations  in  Gastric  Acidity  in  ncalth. 

preceding  generations,  the  frequency  with  which  the  dia- 
gnosis is  missed  at  the  present  day,  and  the  numerous 
difficulties  experienced  in  collecting  and  recording  medical 
pedigrees,  it  seems  probable  that  the  true  incidence  of  posi- 
tive family  liistories  would  be  appreciably  liigher  than  10 
per  cent. 

In  respect  of  correlated  variations  we  find  again  and 
again  that  the  victim  of  duodenal  ulcer  conforms  to  a dis- 
tinct physical  and  psychological  type,  in  which  a lean, 
muscular,  energetic,  and  often  robust  habit  of  body  accom- 
panies a propensity  for  restless  and  conscientious  activity 


DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN  4433 
or  a worrying  disposition.  Radiologically  the  stomach  is 
commonly  of  the  short,  ‘steer-horn’  type,  active  and 
quickly  emptying.  Even  if  it  be  admitted,  as  it  must  be, 
that  external  influences,  including  occupational  stress,  over- 
smoking, the  colder  seasons  of  the  year,  and  infection,  are 
essential  additional  or  determining  factors,  it  would  yet 
seem  just  to  claim  that  a native  hyperchlorhydria,  in  con- 
cert with  the  other  physical  and  psychological  variants 
described,  furnishes  just  such  a deflexion  from  the  mean  of 
healthy  function  as  would  be  calculated  to  predispose  to 
this  disease. 

The  Pernicious  Anaemia  Diathesis 
In  the  series  of  healthy  students  referred  to  above  there 
were  four  whose  stomachs  were  found  to  be  devoid  of  all 
secretion  of  hydrochloric  acid.  Hurst  [2]  has  argued  that 
a considerable  proportion  of  all  cases  of  pernicious  anaemia 
are  consequent  upon  an  inborn  or  constitutional  achylia. 
Achylia  gastrica  is  almost  constant  in  this  disease  and  is 
now  generally  accepted  as  an  essential  aetiological  factor. 
Pernicious  anaemia  may  also  complicate  the  artificial 
achlyia  of  gastrectomy.  In  support  of  his  view  Hurst 
adduces:  (I)  the  occurrence  of  achylia  in  a small  proportion 
of  healthy  individuals;  (2)  the  more  frequent  occurrence  of 
achylia  in  the  families  of  patients  with  pernicious  anaemia; 
and  (3)  some  striking  examples  in  which  pernicious  anaemia 
has  appeared  in  two  or  more  members  or  generations  of  one 
fnmily.  There  are,  furthermore,  certain  correlated  varia- 
tions which  lend  colour  to  the  constitutional  hypothesis 
in  the  case  of  pernicious  anaemia.  Addison  [8]  noted  that 
it  occurred  ‘chiefly  in  persons  of  a somewhat  large  and 
bulky  frame,  and  with  a strongly  marked  tendency  to  the 
formation  of  fat'.  Draper  [9),  with  anthropometric  studies, 
demonstrates  a type  of  chest,  generally  deep,  vide,  and  short, 
which  he  claims  as  peculiar  to  victims  of  the  disease. 

Thus  in  two  very  diverse  conditions,  duodenal  ulcer  and 
pernicious  anaemia,  we  find  support  for  the  idea  of  con- 
stitutional predisposition  (a)  in  the  family  history,  (b)  in  the 
association  of  certain  correlated  variations  (which  proclaim 

F f 


434  DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN 
a ‘type’  but  do  not  in  themselves  explain  the  predisposi- 
tion), and  (c)  in  the  occurrence  of  remarkable  biochemical 
variations  which  (in  the  light  of  recent  research)  go  a long 
way  towards  explaining  the  liability.  If  it  were  possible  to 
chart  in  a similar  manner  the  degrees  of  variability  in  respect 
of  other  functions  of  the  body  it  is  probable  that  we  should 
discover  divergencies  comparable  to  those  shown  in  the 
case  of  gastric  acidity,  and  that  at  the  two  extremes  we 
should  find  an  increased  and  diminished  liability  to  certain 
types  of  injury  or  disease. 

Is  it  not  probable  that  the  metabolism  of  purine  bodies, 
if  it  could  be  measured  and  charted  in  the  same  graphic  way, 
would  be  found  in  a long  series  of  young  and  healthy  indi- 
viduals to  show  wide  variations,  and  among  the  extremes 
might  we  not  anticipate  a pronounced  liability  to,  or  im- 
munity from,  gout  in  later  life?  Some  day  it  may  even 
become  possible  to ' measure ' the  susceptibility  of  the  young 
to  tuberculosis  just  as  we  can  in  some  degree  already,  with 
the  Schick  and  Dick  tests,  reveal  a great  or  little  liability 
to  diphtheria  or  scarlet  fever.  In  this  event  it  is  scarcely 
to  be  doubted  that,  together  with  familial  liability  or 
freedom  and  in  association  with  distinctive  physical  types, 
we  should  find  a parallel  positiveness  or  negativeness  in 
our  tests. 

Idiosyncrasies  to  foodstuffs  and  drugs,  whatever  their 
intimate  physiological  basis  may  be,  are  in  the  same  cate- 
gory as  diatheses.  Indeed  Hutchinson  described  idiosyn- 
crasy, as  Rolleston  [10]  has  lately  reminded  us,  as  * diathesis 
brought  to  a point’. 

Whatever  part  external  stresses  may  play,  variations  in 
psychological  equipment  undoubtedly  do  much  to  deter- 
mine the  degree  of  liability  to  the  common  neuroses  and 
psychoses. 

The  study  of  constitution  and  diathesis  is  one  of  abound- 
ing interest  and  real  practical  value.  We  must  needs  observe 
the  temperament,  peculiarities,  and  individual  reactions  of 
our  patients  and  of  their  near  relatives  with  a constant 
watchfulness  if  we  are  to  preserve  a just  balance  in  the 
departments  of  diagnosis,  prognosis,  and  treatment.  In 


DIATHESIS,  OR  VARIATION  AND  DISEASE  IN  MAN  435 
assessing,  in  respect  of  any  disease  but  especially  of  the 
more  chronic  forms,  the  aetiological  contribution  of  sex, 
season,  occupation,  environment,  and  infection,  we  can 
never  afford  to  neglect  the  abiding  contribution  of  original 
hereditary  endowment.  There  are  better  inspirations  to 
thoughtful  medicine  to  be  found  in  the  Origin  of  Species 
than  in  a modern  text-book  of  bacteriology.  To  physiology, 
let  me  repeat,  we  are  surely  entitled  to  look  for  future  help 
in  the  shape  of  organized  research  into  the  whole  problem 
of  human  variability.  Few  problems  offer  better  prospects 
for  a fruitful  partnership  between  physiology  and  clinical 
medicine.  The  proper  study  of  mankind,  in  sickness  and 
in  health,  is  always  man. 

REFERENCES 

1.  Hutchinson,  J.:  The  Pedigree  of  Disease.  London,  1884. 

2.  Hurst,  A.  F.:  Medical  Essays  and  Addresses . London,  1024. 

3.  Gakrod,  A.  E.s  The  Inborn  Factors  in  Disease.  Oxford,  1931. 

4.  Huxley,  T.  H.:  Man's  Place  in  Nature  and  Other  Essays.  Lon- 

don, 1006. 

5.  Ryle,  J.  A.:  Clinical  Journal,  1931,  lx.  73. 

6.  Bennett,  T.  I.,  and  Ryle,  J.  A.:  Guy's  Hasp.  Pep.,  1021,  Ixxi. 

286,  and  Ryle,  J.  A.:  Gastric  Function  in  Health  and  Disease. 

London, 1026. 

7.  Ryle,  J.  A.:  Lancet,  1923,  i.  327. 

8.  Addison,  T.:  Collection  of  the  Published  Writings.  New  Syden- 

ham Society,  1868. 

9.  Draper,  G.:  Human  Conslitulion.  London  and  Philadelphia, 

1024. 

10.  Rolleston,  H.  D.:  Idiosyncrasies,  London,  1927. 


XXXV 


OPENING  REMARKS  AT  A DISCUSSION  ON 
RESEARCH  IN  CLINICAL  MEDICINE1  . 

We  may  presume  that  the  main  motive  for  the  present  de- 
bate on  research  in  clinical  medicine  is  a prevailing  sense  of 
dissatisfaction  with  the  achievements  of  clinical  inquiry  or 
with  the  conditions  upon  which  achievement  has  to  depend. 
I believe  it  no  exaggeration  to  say  that  we  are  all  at  this 
moment  alive  to  the  existence  of  disturbing  and  retrograde 
tendencies  in  modern  medicine.  In  the  department  of 
diagnosis,  early  specialization  and  the  advent  of  numerous 
physical  and  chemical  methods,  which  at  first  promised — 
and  in  some  degree  have  proved  competent — to  enhance  the 
science  and  accuracy  of  clinical  study,  have  brought  disap- 
pointment in  their  train,  have  hampered  the  natural  evolu- 
tion of  common  observation  and  common  sense,  and  fostered 
faulty  methods  and  an  uncritical  attitude  in  experiment. 
In  the  department  of  therapeutics,  although  there  have  been 
some  notable  discoveries,  the  same  uncritical  attitude  and 
commercial  enterprise  have  between  them  encouraged  an 
empiricism  quite  unworthy  of  our  age.  In  the  department 
of  prognosis  there  has  not  only  been  no  general  advance, 
but  an  actual  loss  of  competence  through  neglect  of  the 
study  of  what  may  be  called  the  natural  history  of  disease  in 
man.  The  time  has  come  for  a reawakening  of  interest  in 
medical  philosophy.  Clinical  practice  will  receive  a strong 
stimulus  to  improvement  when  the  methods  of  clinical 
science  are  better  determined.  It  is  part  of  the  function 
of  philosophy  to  direct  or  determine  method. 

Apart  from  a general  and  largely  silent  discontent  there 
have  also  been  two  important  pronouncements  of  late 
which  I cannot  but  hold  responsible  in  some  part  for  the 
inauguration  of  this  discussion.  I refer  to  papers  by  Sir 
Thomas  Lewis  on  ‘Research  in  Medicine,  Its  Position  and 
Its  Needs’  (Brit.  Med.  Joum.,  15  March  1930),  and  by  Sir. 

* Ptoc.  of  the  Royal  Soc.  of  Med.,  1030,  ndv.  151. 


RESEARCH  IN  CLINICAL  MEDICINE  437 

Wilfred  Trotter  on  * Observation  and  Experiment  and  their 
Use  in  the  Medical  Sciences*  (Brit.  Med.  Journ.,  26  July 
1930).  I am  sure  that  many,  like  myself,  must  have  drawn 
inspiration  from  these  papers  and  that  there  is  much  to  be 
found  in  them  on  which  to  base  the  general  scheme  of  our 
discussion.  More  recently,  and  since  my  own  thoughts  were 
put  to  paper,  Lord  Moynihan  has  handled  the  same  topic  in 
his  address  at  the  Banting  Research  Institute. 

My  first  duty  as  opener  is  to  indicate  the  boundaries  of 
the  subject,  and  to  suggest  what  aspects  of  it  we  may  most 
profitably  consider.  I would  suggest  that  we  might  consider 
in  turn  the  meaning,  the  methods,  and  the  scope  of  modern 
clinical  research  and  the  opportunities  which  are  at  present, 
or  should  ideally  be,  provided  for  its  proper  conduct. 

The  Meaning  of  Clinical  Research 

Of  the  department  of  progressive  medicine  whose  needs 
he  is  voicing.  Sir  Thomas  Lewis  writes: 

‘It  may  be  termed  clinical  science.  This  science  seeks,  by  observa- 
tion and  otherwise,  to  define  diseases  as  these  occur  in  man  j it  at- 
tempts to  understand  these  diseases  and  their  many  manifestations, 
and  here  especially  makes  frequent  use  of  the  experimental  method. 
It  makes  definite  experiments  upon  disease  or  watches  the  effects  of 
experiment  conducted  by  injuries,  however  these  arise;  it  culls,  or 
actually  creates,  and  uses  physiological  and  pathological  knowledge 
Immediately  related  and  applicable  to  the  diseases  studied.  Its  value 
has  been  abundantly  and  frequently  displayed  in  this  country  by 
such  experimental  clinicians  as  Ferrier,  Horsley,  Mackenzie,  and 
Head.  The  very  mention  of  these  names  is  in  effect  a definition  of 
the  science  that  is  in  mind.  Their  work  was  not  work  that  could  be 
delegated  to  laboratories;  it  was  inspired  and  sustained  by  direct 
contacts  with  disease ; it  was  carried  through  in  very  large  or  cliief 
measure  by  observations  on  sick  people.' 

In  defining  the  meaning  of  clinical  research  we  cannot,  I 
think,  do  better  than  follow  this  lead.  Research  in  clinical 
medicine  is  not  pathological,  bacteriological,  or  biochemical 
research.  These  are  concerned  with  the  study  of  the  agents, 
the  processes  and  the  consequences  of  disease  in  man  under 
the  conditions  of  the  laboratory,  and  often  with  the  lielp  of 
experiments  in  animals.  Clinical  science  should  rather  be 


438  OPENING  REMARKS  AT  A DISCUSSION 
considered  as  a branch  of  the  science  of  human  biology.  It 
studies  the  behaviourism  of  disease  in  man,  or  perhaps  it 
would  be  more  correct  to  say  of  man  in  disease.  It  observes, 
records,  and,  when  possible,  measures  the  processes  of  disease 
as  they  occur  in  the  living  subject,  and  within  certain  limi- 
tations it  may  control,  modify,  or  reproduce  these  processes 
for  purposes  of  detailed  study. 

The  Methods  of  Clinical  Research 
The  methods  of  all  scientific  research,  in  their  broadest 
subdivision,  are  either  observational  or  experimental.  Some 
sciences,  such  as  zoology  and  geology,  are  essentially 
observational.  Others,  such  as  physics  and  physiology,  have 
depended  for  their  progress  almost  entirely  upon  experiment. 
The  great  scientists  like  Harvey  and  Darwin  have  wherever 
possible  employed  both  methods,  calling  one  in  support  of 
the  other.  While  it  was  a particular  instruction  of  Harvey’s 
that  we  should  ‘search  and  study  out  the  secrets  of  Nature 
by  way  of  experiment’,  in  all  his  work  and  elsewhere  in 
discussing  method  he  couples  observation  with  experiment, 
knowing  them  both  to  be  indispensable  in  the  biological 
sciences  and  complementary  to  one  another.  The  great 
clinical  scientists  have  all  realized  this,  but  with  the  growth 
of  the  ancillary  sciences  of  physiology  and  pathology  the 
natural  tendency  has  been  in  the  direction  of  a division  of 
labour,  the  demands  of  experiment  claiming  certain  faculties 
and  an  expenditure  of  time  which  left  little  opportunity  for 
observational  study,  and  the  busy  life  of  the  physician  (the 
student  of  tj>vats  or  nature,  as  his  name  implies)  allowing 
small  scope  for  experiment.  Scientifically  it  has  been  the 
misfortune,  not  the  fault,  of  the  physician  that  he  has 
always  had  to  expend  a disproportionately  large  part  of  his 
energies  in  the  treatment  and  management  of  patients.  As 
Lewis  insists,  the  pursuit  of  curative  medicine  necessarily 
conflicts  at  many  points  with  the  advancement  of  scientific 
medicine.  Nevertheless  many  of  the  greatest  contributions 
to  medicine— or  shall  we  call  it  physic,  the  science  of  the 
physician  or  naturalist  ? — have  been  due  to  members  of  the 
observational  school  who  were  practitioners  of  medicine. 


ON  RESEARCH  IN  CLINICAL  MEDICINE  439 
Hippocrates,  Sydenham,  Bright,  Laennec,  and  Addison  were 
among  the  foremost  exponents  of  this  school  and,  although 
he  cites  them  as  examples  of  the  experimental  clinician,  I 
am  sure  Lems  would  admit  that  Mackenzie  and  Head  owed 
at  least  as  much  of  their  achievement  to  the  method  of 
observation. 

Both  Lewis  and  Trotter  in  the  papers  referred  to  would 
seem  to  imply  that  the  great  and  spacious  days  of  observa- 
tional medicine  are  almost  numbered  and  that  the  future  is 
all  for  experiment.  Here  I cannot  find  myself  in  full  agree- 
ment with  them.  With  improvements  in  our  methods  of 
training  and  observation,  I believe  it  should  be  possible  to 
add  to  our  knowledge  of  man  in  disease  contributions  os 
important  as  any  of  those  made  in  the  past  and  often 
equivalent  in  practical  advantage  to  those  supplied  by  ex- 
periment. Further,  whereas  the  fields  open  to  the  observa- 
tional physician— difficult  though  they  be  to  encompass — 
are  many  and  varied,  the  scope  of  experiment  must,  by  the 
dictates  of  humanity,  remain  somewhat  strictly  limited. 

At  this  point,  perhaps,  wc  should  demand  a clear  ruling 
as  to  where  observation  ends  and  experiment  begins.  The 
use  of  instruments  of  precision,  for  instance,  cannot  be  held 
to  turn  observation  into  experiment.  The  stethoscope,  the 
sphygmomanometer,  the  electrocardiograph  have  all  im- 
proved our  observational  capacity,  but  to  study  a patient 
or  a series  of  patients  with  their  aid  constitutes  not  an 
experiment  but  a refinement  of  the  observational  method. 
The  same  may  be  said  of  radiology  and  the  innumerable 
biochemical  tests  which  have  for  their  purpose  the  measure- 
ment of  vital  phenomena  and  their  comparison  with  normal 
standards.  If,  on  the  other  hand,  we  study  the  effects  of  a 
new  drug  on  the  action  of  a disordered  heart  with  the  aid  of 
the  electrocardiograph ; if  we  strive  to  reproduce  a gastric 
pain  artificially  and  simultaneously  observe  the  movements  • 
of  the  stomach  on  the  fluorescent  screen ; if  we  watch  the 
capillary  responses  to  applications  of  heat  or  cold  or  the 
injection  of  a drug ; if  we  invent  and  test  a new  operation ; 
then  we  are  employing  the  experimental  method.  In  the 
one  case  wc  are  observing  the  casual  experiments  of  Nature ; 


440  OPENING  REMARKS  AT  A DISCUSSION 
in  the  other  we  are  actually  promoting  small-scale  experi- 
ments of  our  own. 

When  we  come  to  a consideration  of  the  projects  and  the 
more  intimate  procedures  open  to  the  observational  physi- 
cian and  to  a comparison  of  these  with  those  at  present  avail- 
able for  the  experimentalist,  I think  we  must  agree  that  the 
former  still  has  the  broader  programme  before  him.  Just  as 
in  animal  biology  the  modem  trend  is  in  the  direction  of 
studying  behaviour,  oecology,  and  genetics  in  the  open,  as 
opposed  to  laboratory  inquiry,  so,  in  my  belief,  the  next  trend 
in  clinical  medicine  (or  the  biology  of  man  in  disease)  will 
be  in  the  direction  of  a study,  at  once  broader  and  more 
intimate,  of  behaviour,  personality,  idiosyncrasy,  vital 
reactions,  and  genetic  factors  in  our  living  patients,  while 
experimental  inquiry  (always,  I trust,  co-operative),  in  the 
hands  of  an  expert  few,  runs  a parallel  course.  Until  new 
instruments  of  precision  come  to  trial,  or  some  new  depar- 
ture in  pharmacology  or  surgery  is  signalled,  the  methods 
of  human  experiment  at  our  disposal  are,  it  seems  to  me, 
conspicuously  few. 

The  Scope  of  Clinical  Research 

The  contributions  of  the  older  physicians  were  chiefly  in 
respect  of  the  broader  natural  history  of  disease.  By  careful 
study  of  symptoms  and  signs,  and  at  a later  date  by  correla- 
tion of  the  phenomena  observed  in  life  with  the  changes 
found  in  the  cadaver,  they  established  a classification  of 
diseases  and  some  reasonable  interpretations  of  symptoms. 
They  also  paid  much  attention,  though  of  a superficial  kind, 
to  the  influence  of  temperament,  heredity,  and  environment. 
They  often  wielded  well  the  tool  of  inductive  reason.  In 
their  tasks  they  were  chiefly  hampered  by  their  limited 
knowledge  of  normal  physiology  and  by  their  lack  of  precise 
methods  of  observation.  Later  generations  have  recovered 
the  ground  they  trod,  adding  and  improving  here  and  there 
by  new  and  more  accurate  observations,  or  by  the  interpre- 
tation of  old  observations  on  the  basis  of  fresh  physiological 
and  pathological  knowledge.  New  diseases  continue  even 
now  to  be  discovered  and  described  by  the  observational 


ON  RESEARCH  IN  CLINICAL  MEDICINE  441 
method.  Important  syndromes,  such  as  those  proclaiming 
a coronary  thrombosis  or  a sub-arachnoid  haemorrhage, 
have  only  lately  been  established  and  analysed.  A more 
minute  analysis  of  morbid  phenomena  continues  to  make 
our  appreciation  of  the  natural  history  of  the  old  diseases 
more  intimate.  Where  laboratory  research  has  had  an  appli- 
cation this  has  generally  been  promptly  utilized.  Where 
laboratory  research  has  led  astray  or  has  endeavoured  to 
simplify  when  simplification  was  impossible,  the  clinical  ob- 
server has  often  supplied  the  corrective.  I would  maintain 
that  his  task  is  not  nearly  ended. 

Certain  special  fields  for  clinical  research  at  once  com- 
mend themselves.  The  wide  realm  of  subjective  symptoma- 
tology,  which  constitutes  a major  part  of  morbid  physiology 
—and,  let  it  be  remembered,  symptoms  are  the  earliest 
phenomena  of  disease — is  still  largely  unexplored,  if  we 
except  certain  important  contributions  to  the  study  of  pain. 
We  ought  by  now  to  have  more  accurate  information  in  our 
possession  about  nausea,  heartburn,  the  dyspnoeas,  and 
the  many  varieties  of  aches  in  body,  head,  and  limb.  It 
should  be  possible  to  determine  with  greater  precision  the 
nature  of  those  abdominal  pains  which  nowadays  lead  so 
constantly  to  fruitless  surgical  intervention.  Symptoms  as 
expressing  particular  disturbances  of  function  and  not  as 
listed  characteristics  of  a particular  disease  are  clamouring 
for  organized  research.  The  influence  of  constitution  on 
the  incidence  and  course  of  the  chronic  diseases  is  just  be- 
ginning to  attract  fresh  interest,  which  should  go  far  to 
provide  a stimulus  for  future  research,  and  not  exclusively 
along  the  anthropometric  lines  laid  down  by  Draper.  In 
aetiological  studies,  socio-medical  surveys  of  populations 
determined  by  age,  sex,  occupation,  geography,  or  otherwise, 
and  requiring  the  collaboration  of  physician,  social  worker, 
and  statistician,  should  have  not  a little  to  teach  us  (vide 
Chapter  XXXVI).  In  therapeutics  there  is  much  waiting 
to  be  done,  but  almost  more  to  be  undone.  It  should  not 
have  been  necessary  to  wait  a quarter  of  a century  to 
discover  by  slow  and  bitter  experience  that  the  greater 
part  of  vaccine-therapy,  as  prescribed  or  practised  by 


442  OPENING  REMARKS  AT  A DISCUSSION 
specialists  having  little  or  no  acquaintance  with  the  natural 
history  of  disease  in  man,  was  a delusion  unworthy  of  a 
scientific  profession.  With  combined  experiment  and  ob- 
servation in  accredited  hospitals  by  trained  workers  it 
should  be  possible  to  decide  within  a comparatively  short 
time  what  is  good  and  what  bad  in  the  serum  treatments 
and  chemotherapies  at  present  advocated  in  acute  bacterial 
disease,  and  what  is  potent  and  what  useless  among  the 
endocrine  preparations.  The  principles  of  prognosis  in  acute 
bacterial  infections  and  other  anxious  maladies  should  by 
careful  observation  become  more  surely  established.  Neuro- 
logy has  in  recent  times  been  greatly  and  rapidly  advanced 
mainly  by  observation,  but  partly  also  by  surgical  experi- 
ment. In  the  realm  of  morbid  psychology,  which  owes  much 
of  its  rapid  growth  to  the  observational  method,  there  is 
ample  scope  for  further  research,  and  by  this  means  many 
diseases  and  disorders  at  present  in  receipt  of  vague  physical 
labels  will  eventually  find  their  true  category'. 

I have  mentioned  but  a few  departments  of  medicine 
awaiting  the  broom  of  careful  observational  research.  In 
several  instances  cxperimdnt  should  lend  a helping  hand. 
In  each  instance  it  seems  reasonable  to  hope  that  research 
will  bring  practical  advantage.  But  clinical  research  need 
not  necessarily  be  utilitarian.  There  are  many  diseases  of 
obscure  causation  which  are  worth  studying  for  their  own 
sake  as  natural  phenomena.  Much  research  in  modem 
physiology  is  devoid  of  immediate  application,  and  for  those 
who  have  no  humanitarian  interest  in  medicine  and  can 
devote  their  lives  to  such  work  clinical  science  can  also 
provide  a wealth  of  problems.  Among  the  rarer  diseases  and 
peculiarities  there  are  some  which  provide  for  the  experi- 
mentalist material  especially  suited  to  his  needs. 

The  Opportunities  tor  Clinical  Research 

We  come  lastly  to  the  question  of  opportunity.  There 
can  be  no  disputing  the  truth  of  Sir  Thomas  Lewis’s  conten- 
tion that  at  present  there  is  no  adequate  provision  and  no 
adequate  encouragement  for  the  young  man  who  would 
devote  his  life,  or  part  of  it,  to  clinical  research.  The  step- 


ON  RESEARCH  IN  CLINICAL  MEDICINE  443 
ping-stones  whereby  he  must  cross  the  stream  between 
qualification  and  economic  independence  in  medicine  are 
customarily  house-appointments,  junior  staff  appointments, 
and,  for  a shorter  or  longer  period  of  lean  years,  an  assis- 
tant physicianship  at  a teaching  hospital.  Alternatively  he 
makes  general  practice  or  specialism  his  goal.  If  he  embark 
during  any  part  of  his  probationary  period  upon  a useful 
piece  of  research  he  is  seldom  if  ever  in  a position  to  give 
it  his  full  time  or  to  find  free  access  to  the  appropriate 
material.  As  a rule  he  does  not  see  enough  patients.  As  soon 
as  practice — -which  is  the  necessary  aim — begins  to  arrive 
his  outlook  alters,  his  time  is  consumed,  and  his  hopes  of 
scientifically  productive  work  diminish.  A research  grant 
may  help  him  here  and  there,  but  no  one  and  no  institution 
offers  him  security.  Physiology  and  pathology,  none  too 
well  endowed  themselves,  offer  better  economic  opportunity 
than  clinical  science. 

It  is  doubtful,  however,  whether  ‘curative’  medicine  and 
‘progressive’  medicine,  as  Lewis  calls  them,  can  ever  be 
divorced  as  he  would  wish.  No  one  can  conduct  research 
on  patients  who  are  not  under  his  own  care,  and  no  one  can 
have  patients  under  his  care  for  research  purposes  and  not 
treat  them.  It  should,  however,  be  possible  for  a promising 
man  to  be  relieved  of  the  absolute  necessity  of  private  prac- 
tice and  much  crippling  routine  for  a term  of  years,  and, 
in  special  cases,  through  his  working  life.  The  professorial 
units  with  their  assistantships  do  not  quite  fulfil  the  require- 
ments. Special  hospitals  or  wards  for  selected  men  and 
devoted  to  research  purposes  would  defeat  their  own  ends 
through  creating  a wrong  environment,  a new  kind  of  ultra- 
specialism,  and  a separation  from  the  healthy  criticism  of 
men  engaged  in  teaching  and  practice. 

In  the  scheme  for  research  physicians  as  forecast  by  Sir 
Thomas  Lewis  and  initiated  by  the  Medical  Research  Council 
there  are  many  points  for  criticism,  but  there  is  the  germ  of  a 
good  idea.  To  become  a physician  at  all  (whether  we  use  the 
term  in  its  oldest  and  best  sense  as  meaning  a student  of 
nature,  or  in  its  modern  interpretation  as  a healer  of  the 
sick)  requires  many  years  of  initiation  in  a school  far  harder 


•444  OPENING  REMARKS  AT  A DISCUSSION 
than  the  schools  of  physiology  and  pathology,  involving 
constant  contact  with  large  numbers  of  patients.  Only  from 
such  experience  can  fruitful  ideas  and  a proper  balance  be 
derived;  there  is  no  short  cut.  Yet  Lewis  requires  that 
his  men  should  be  young  nnd  that  they  should  be  relieved, 
from  the  beginning,  of  the  gruelling  apprenticeship  of  out- 
patient work  and  word-teuchingand  forbidden  that  intimate 
school  of  private  practice  wherein  most  of  us  find  our  oppor- 
tunities of  seeing  disease  in  its  earlier  stages  and  more  active 
phases,  of  examining  intelligent  patients  under  favourable 
conditions  of  privacy  nnd  in  their  natural  environment,  and 
so  of  gathering,  in  my  firm  conviction,  our  richest  crumbs  of 
instruction  and  inspiration.  Personally  I should  like  to  see 
a vacancy  declared  from  time  to  time  at  the  teaching  hospi- 
tals for  an  additional  assistant  physician,  the  appointment 
to  be  an  open  one  nnd  filled  only  if  a man  of  outstanding 
merit  is  forthcoming.  The  post  should  supply  a general 
medical  out-patient  day,  a few  beds,  and  access  to  all 
material  in  the  hospital  of  use  to  his  self-instruction  and 
research ; with  certain  definite  restrictions  in  respect  of  time 
and  fees,  and  (except  in  the  case  of  acute  disease)  within  the 
precincts  of  the  hospital,  he  should  be  allowed  to  see  private 
patients  referred  to  him  by  colleagues  familiar  with  his 
interests  and  his  needs ; the  appointment  should  be  for  five 
years  in  the  first  instance  and  then  either  renewable  in- 
definitely or  convertible,  perhaps,  to  an  honorary  assistant 
physicianship  of  the  usual  type;  the  salary  should  be  com- 
mensurate at  least  with  those  accorded  to  men  of  junior 
professorial  rank  and,  in  the  event  of  continuance  of  the 
appointment  on  a whole-time  basis,  should  rise  to  equal 
those  accorded  to  full  professors.  Such  a research  physician, 
although  probably  chiefly  concerned  with  one  or  two  types  of 
disease,  must  have  access  to  all  types,  must  work  in  an  atmo- 
sphere of  disease  considered  from  ail  points  of  view,  and 
must  be  in  contact  with  senior,  contemporary,  and  junior 
colleagues  willing  and  eager  to  help  or  criticize.  Whatever 
previous  training  he  may  have  had  in  physiological  or  other 
laboratory  method  he  should  have  held,  as  an  introduction 
to  the  problems  of  man  in  disease,  house-appointments  for 


ON  RESEARCH  IN  CLINICAL  MEDICINE  445 
a year  or  two  at  least,  and  for  a period  of  not  less  than  two 
or  three  years,  a medical  registrarship  or  tutorship,  or  have 
served  a like  period  at  special  institutional  medicine  or  in 
practice.  In  the  selection  of  candidates  credit  should  be 
given  for  a broad  earlier  education  and  particularly  for  some 
grounding  in  philosophy,  logic,  or  psychology  as  against 
purely  technical  abilities  or  an  uninterrupted  scientific 
education  from  the  school  period.  Qualities  as  physician  or 
naturalist  should  be  allowed  at  least  as  strong  a claim  as 
qualifications  for  research  in  other  spheres.  A scholarly 
heredity  should,  by  Galtonian  doctrine,  be  considered  a very 
distinct  advantage. 

Lewis  has  also  reviewed  the  possibilities  of  Clinical  Science 
as  a University  subject,  and  there  is  much  to  be  said  in 
favour  of  his  advocacy. 

These  matters  deserve  our  serious  consideration,  and 
the  more  so  because  the  Medical  Research  Council  are 
fully  alive  to  the  importance  of  clinical  research  and  arc 
lending  it  the  help  of  their  endowments.  The  problems 
which  it  is  their  desire  to  solve  are  our  daily  problems.  It  is 
natural  that  we  should  wish  to  see  them  wisely  approached. 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER1 


All  diseases  of  high  incidence  may  be  said  to  have  a ‘social’ 
as  well  as  an  ‘individual*  pathology.  Where  the  application 
of  knowledge  to  the  practical  purposes  of  prevention — 
as  distinct  from  diagnosis  and  treatment — is  concerned, 
social  pathology  is  clearly  more  important  than  human 
pathology  in  its  more  usual  and  restricted  sense.  The 
two  sciences  should  be  more  closely  integrated.  The  re- 
searches of  the  social  pathologist  are  related  to  ultimate 
causes,  and  more  particularly  to  those  environmental, 
domestic,  occupational,  economic,  habitual,  and  nutritional 
factors  without  which  the  intimate  (or  specific)  causal  factors 
cannot  find  their  opportunity.  They  are  concerned  with 
the  trends  of  mortality  and  morbidity  in  the  community  as 
a whole  and  its  component  groups,  and  with  the  particular 
influence  upon  these  of  differing  social  conditions.  The 
methods  of  social  pathology  include:  (i)  the  social  post- 
mortem examination  conducted  by  means  of  statistical 
analyses  of  official  mortality  figures,  and  correlations  of 
these  with  measurable  social  influences;  (ii)  morbidity 
studies  with  similar  correlations ; (iii)  planned  ad  hoe  socio- 
medical surveys;  and  (iv)  social  experiments.  By  such 
methods  not  only  the  extent  and  trends  and  the  con- 
sequences of  community  diseases,  but  also  their  aetiology 
can  be  studied  as  profitably  as  their  specific  aetiology  and 
intimate  morbid  processes  are  studied  in  the  ward,  the 
dead-house,  and  the  laboratory. 

From  mortality  studies  we  know  that  the  standardized 
death-rate  for  pulmonary  tuberculosis  rises  steeply  in 
passing  from  the  higher  to  the  lower  socio-economic  groups 
and  that  it  is  approximately  twice  as  high  in  Social  Class  V 
as  in  Social  Class  I (Registrar-General’s  classification).  The 

1 Based  on  an  address  given  at  the  annual  meeting  of  the  Royal  Sani- 
tary Institute  (Joum.  of  the  Royal  Sanitary  InsL  1946,  Isvi.  277). 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  447 
same  is  true  for  infant  mortality,  which  at  the  census  period 
1030-2,  was  four  and  a half  times  higher  in  Social  Class  V 
than  in  Social  Class  I,  the  intervening  classes  showing 
intermediate  figures.  Valvular  heart  disease,  the  syphilitic 
diseases,  gastric  ulcer — all  show  the  same  discrimination 
against  the  lower  income  groups,  whose  environmental, 
nutritional,  educational,  and  other  advantages  still  remain 
grossly  inferior  to  those  of  the  professional  and  more 
privileged  groups.  Even  cancer — where  the  upper  ali- 
mentary tract  and  the  skin  are  concerned — discriminates 
against  working-class  populations.  Tuberculosis  mortality, 
although  continuing  to  fall,  remains  closely  correlated  with 
living  conditions  and  accommodation  and  with  certain 
occupations,  and  it  reacts  adversely  to  war  conditions  and 
any  decline  in  nutritional  standards.  Certain  occupations 
carry  with  them  an  all-causes  mortality  grossly  in  excess 
of  the  anticipated  mortality  for  the  male  population  as  a 
whole,  while  others  give  a better  expectation  of  life.  Some 
lethal  diseases  discriminate  against  the  higher  income  groups 
and  against  certain  professions;  among  these  coronary 
artery  disease  is  a notable  example.  The  social  pathology 
of  all  these  and  many  other  common  diseases  is  clearly  as 
worthy  of  study  and  development  as  are  those  branches  of 
human  pathology  which  concern  themselves  rather  with 
the  causes,  manifestations,  course,  and  end-results  of 
disease  as  it  affects  the  individual. 

Numerous  papers  have  appeared  in  recent  years  bearing 
upon  the  social  pathology  of  rheumatic  fever,  which  remains, 
during  the  earlier  decades  of  life  in  these  islands  and  in 
many  other  countries,  one  of  the  most  lethal  and  crippling 
of  our  prevailing  community  diseases.  A review  of  the 
present  state  of  our  knowledge  would  seem  timely,  particu* 

riy  ha  ring  regard  for  impending  social  changes  and  the  large 
rehousing  programmes  with  which  we  are  confronted.  I have 
confined  myself  in  the  main  to  the  experience  of  this  country. 

Definitions 

"We  may  include  under  the  general  title  of  rheumatic 
fever  the  acute  and  so-called  sub-acute  rheumatisms  of 


448  THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER 
childhood,  adolescence,  and  early  adult  life ; juvenile  chorea ; 
and  rheumatic  carditis  occurring  with  or  without  definitive 
articular  manifestations,  rheumatic  nodules  or  chorea.  We 
must  accept  that  diagnosis  is  not  always  easy,  and  that, 
without  the  development  of  a cardiac  lesion,  certain  transi- 
tory fevers  and  pains  cannot  with  full  assurance  be  included 
in  our  category. 

Within  the  orbit  of  social  pathology,  wc  can  properly 
consider  studies  bearing  upon  mortality,  morbidity,  and  all 
those  influences  of  environment  and  socio-economic  status 
to  which  locality,  housing,  crowding,  poverty,  and  nutri- 
tional and  educational  defects  make,  or  may  mnke,  their 
contribution.  Since  the  family  is  the  smallest  social  unit, 
the  influence  of  familial  predisposition  may  also  be  included. 
Although  they  play  their  part  in  aetiology,  age  and  sex 
might  be  regarded  as  individual  rather  than  social  factors, 
and  yet  both  of  them  circumscribe  n social  group  within  the 
general  population.  Geography,  climate,  and  season  are 
general  extrinsic  influences  which  must  be  considered  in  all 
full  aetiological  inquiries.  They  are  not  social  factors,  but 
they  may  impose  different  degrees  of  stress  upon  different 
nations  or  social  groupings. 


The  Size  of  the  Problem 

When  we  come  to  review  the  incidence  of  rheumatic 
fever  and  its  sequels  in  this  country,  we  at  once  find  ourselves 
at  a disadvantage  for  lack  of  morbidity  figures.  Mortality 
cannot  exactly  reflect  morbidity,  and  yet  our  present 
judgements  must  be  largely  based  upon  mortality  records. 
Mortality  studies  in  the  case  of  a disease  with  an  initial  onset 
usually  preceding  death  by  many  years  cannot  inform  us 
accurately  about  the  distribution  or  secular  trend  or  the 
possible  social  and  environmental  associations  of  the 
disease  at  its  inception. 

It  has  been  estimated  (Morris  and  Titmuss)  [1]  that 
there  are  nearly  200,000  cases  of  rheumatic  heart  disease 
at  all  ages  in  this  country.  Parkinson  [2]  suggests  a present 
figure  of  at  least  200,000  cases  of  heart  disease  in  Great 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  -J49 
Britain,  mostly  rheumatic,  between  ages  18  and  41,  and 
(citing  Stocks)  that  the  annual  deaths  in  England  and 
Wales  from  rheumatic  heart  disease  may  be  considered  as  in 
the  neighbourhood  of  1G,000.  Close  upon  100  per  cent,  of 
deaths  from  heart  disease  before  the  age  of  40  are  a con- 
sequence of  rheumatic  carditis,  which  is  second  only  as  a 
cause  of  death  to  pulmonary  tuberculosis  in  females  between 
5 and  45,  and  follows  tuberculosis  and  violence  in  males. 
Before  the  war  it  accounted  for  2 per  cent,  of  all  deaths 
in  England  and  Wales  and  10  per  cent,  of  the  deaths  be- 
tween 5 and  45  [8]. 

Estimates  from  hospital  sources  of  the  proportion  of 
rheumatic  children  developing  heart  disease  have  varied 
between  50  per  cent,  and  90  per  cent.  As  hospitals  are 
concerned  with  the  more  serious  cases,  and  minor  and  ‘sub- 
clinical’  infections  (as  in  the  case  of  pulmonary  tuberculosis) 
are  probably  common  and  must  often  pass  unrecorded  or 
unrecognized,  reliable  estimates  are  not  at  present  possible. 
Bach  ct  al.  [3]  report  that  in  1938  the  London  County 
Council  card  index  of  children  up  to  15  who  were  suffering 
from  or  had  suffered  from  rheumatic  infections,  included 
22,800  children,  or  about  2*0  per  cent,  of  the  child  popu- 
lation. Pre-war  estimates  of  the  incidence  of  rheumatic 
heart  disease  in  school  children  have  varied  between  1 per 
cent,  and  5 per  cent.  In  London  it  was  estimated  that  the 
incidence  of  rheumatic  heart  disease  in  school  children  had 
fallen  from  2 per  cent,  to  0 77  per  cent,  between  1020  and 
1937  [3].  The  incidence  of  the  disease  and  the  deaths  in  the 
early  acute  phase  of  rheumatic  fever  in  children  are  both 
declining.  Hospital  physicians  of  mature  experience  would 
probably  agree  that  serious  initial  attacks  with  polyarthritis, 
pericarditis,  and  hyperpyrexia  have  become  more  rare  in 
their  lifetime,  but  valvular  disease  continues  to  complicate 
many  of  the  less  severe  rheumatic  episodes.  Special  hospi- 
tals, clinics,  schools,  and  other  provisions  are  inadequate  for 
the  needs  of  all  the  damaged  hearts.  The  direct  and  indirect 
costs  of  the  disease  to  the  community  must  be  very  heavy. 
Socially  and  nationally,  the  problem  remains  a large  and 
serious  one. 


450  TIIE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER 


Specific  Factors 

Brief  reference  must  be  mode  to  the  intimate  or  specific 
factors,  as  distinct  from  the  ultimate  factors,  in  aetiology. 

Although  agreement  has  yet  to  be  finally  reached  on  the 
subject,  evidence  steadily  accumulates  in  favour  of  Strepto- 
coccus pyogenes  (or  certain  of  its  serological  types)  as  the 
infective  agent.  Sore  throats,  or  other  infections  of  the 
upper  respiratory  tract,  commonly  precede  the  individual 
rheumatic  attack;  epidemics  of  streptococcal  sore  throat 
in  partially  closed  communities  have  frequently  been  ac- 
companied or  followed  by  epidemics  of  rheumatic  fever 
with  carditis  in  a proportion  of  the  population  at  risk. 
Hospitalized  cases  of  rheumatic  heart  disease  too  commonly 
develop  streptococcal  infections  with  secondary  attacks  of 
carditis  in  the  course  of  ward  epidemics  of  sore  throat. 
Serological  reactions  in  rheumatic  children  support  the 
theory  of  an  initiating  streptococcal  infection.  There  is  also 
some  evidence  that,  while  the  sulphonnmide  drugs  have  no 
good  effect  on  the  rheumatic  attack,  their  prophylactic  use 
may  so  far  protect  against  streptococcal  infections  of  the 
upper  respiratory'  tract  as  to  reduce  significantly  the  inci- 
dence of  rheumatic  recurrences  in  treated,  ns  contrasted 
with  control,  groups.  Barclay  and  King-Lewis  [4],  sum- 
marizing the  American  trials,  quote  these  as  recording  1-2 
per  cent,  of  rheumatic  relapses  in  501  patient  seasons 
(treated  series),  as  compared  with  39-8  per  cent,  of  relapses 
in  505  patient  seasons  (untreated  series).  Experiences  in 
this  country  have  been  less  encouraging. 

There  is  also,  however,  strong  evidence  for  considering  the 
rheumatic  attack  as  a specific  type  of  response  occurring 
at  a susceptible  age  in  the  case  of  individuals  having  an 
inborn  or  acquired  sensitivity  to  a common  agent — an 
agent  which,  in  most  persons,  provokes  a local  reaction 
only,  or  produces  other  types  of  general  response.  The 
rheumatic  attack,  like  other  sensitization  phenomena, 
follows  the  throat  infection,  not  immediately,  but  after  an 
interval  which  may  extend  to  two  or  more  weeks.  Its 
articular  and  cutaneous  phenomena,  like  those  of  serum 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  451 
sickness,  are  transitory.  The  occurrence  of  rheumatic 
families,  with  the  disease  appearing  in  successive  genera- 
tions and  among  individuals  in  those  generations  living  in 
differing  environments,  and  sometimes  even  under  favour- 
able social  conditions  [5],  and  also  the  fact  that  the  majority 
of  children  living  under  unfavourable  conditions  do  not 
acquire  the  disease,  would  favour  the  hypothesis  that — 
as  in  many  other  types  of  infection  and  acquired  illness — 
there  are,  at  the  two  ends  of  the  scale,  types  which  are 
genetically  more  or  less  susceptible  to  infection,  or  more  or 
less  liable  to  develop  a sensitized  state  in  the  presence  of 
infection. 

Bearing  on  the  genetic  factor,  Read  et  al.  [C3  investigating 
the  siblings,  parents,  uncles  and  aunts,  and  grandparents  of 
rheumatic  and  control  children,  found  a significantly  higher 
incidence  in  each  relationship  among  the  former  than 
among  the  latter.  Pickles  [5]  reported  an  interesting  family 
in  which,  among  53  descendants  of  a man — himself  a victim 
of  rheumatic  heart  disease — 23  had  suffered  from  rheu- 
matic fever,  or  had  unmistakable  signs  of  mitral  stenosis. 
Most  of  them  were  prosperous,  well  housed,  and  well  fed. 
Specific  liability,  as  well  as  specific  infection,  must  be 
accorded  fair  consideration. 

Season,  Climate,  and  Geography 

Primary  and  subsequent  attacks  of  rheumatic  fever  arc 
especially  common  in  this  country  in  the  period  October  to 
March — the  period  in  which  the  respiratory  tract  infections 
have  their  highest  incidence.  It  has  been  stated  that  the 
disease  is  more  common  in  northern  than  in  hot  southern 
climates,  but  the  medical  statistics  of  tropical  countries 
arc  at  present  unsatisfactory  and  the  rarity  of  rheumatic 
fever  in  countries  such  as  India  should  not  be  over-empha- 
sized.  In  Madras,  in  1944,  1 was  shown  a number  of  cases 
of  grave  rheumatic  heart  disease  in  a single  ward  of  one 
hospital.  Tlic  squalor  and  poverty  in  many  of  the  working- 
class  districts  of  Indian  cities  are  appalling  and,  although 
seasonal  and  weather  variations  may  be  less  favourable 
there  than  in  our  own  country  to  the  occurrence  and  spread 


452  THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER 
of  catarrhal  infections,  density  of  population  and  living 
conditions  should  be  far  more  so.  Young  [7]  concluded 
from  mortality  studies,  which  revealed  a correlation  be- 
tween the  deaths  from  rheumatic  fever  and  from  heart 
disease  in  the  regions  covered,  that  there  was  a higher 
incidence  of  rheumatic  heart  disease  in  the  western  counties 
than  elsewhere  in  England  and  Wales. 

Social  Factors 

Physicians  have  long  recognized  that  rheumatic  fever 
and  heart  disease  are  relatively  rare  in  private  practice 
among  the  well-to-do,  as  compared  with  their  experience 
of  hospital  practice  and  working-class  populations.  This 
impression  is  supported  by  statistical  investigations  of 
mortality  and  by  special  surveys.  Young  [8];  Miller  [0]; 
the  Medical  Research  Council’s  report  on  ‘Social  Conditions 
and  Acute  Rheumatism’  [10] ; Bruce  Perry  and  Fraser 
Roberts  [11];  Poynton  [12] ; Holland  Clarke  [13] ; and,  more 
xecently,  Morris  and  Titmuss  [1] ; Daniel  [14] ; and  Donovan 
[15] ; have  all  adduced  or  discussed  evidence  which  shows 
that  rheumatic  heart  disease  has  a strong  correlation  with 
poverty,  or,  rather,  with  the  complex  of  adverse  circum- 
stances which  accompany  poverty.  Morris  and  Titmuss  [1] 
show  that  mortality  increases  on  the  whole  with  density  of 
population,  and  that  depressed  rural  districts  return  rates 
as  high  as  the  worst  of  the  big  towns ; they  also  associate 
a subsequent  rise  in  the  mortality  from  rheumatic  heart 
disease  (between  ages  of  5 and  25)  in  the  English  and  Welsh 
county  boroughs  with  the  economic  slump  of  1930-2  [16]. 
London,  Manchester,  Liverpool,  Bristol,  and  Glasgow  have 
been  particularly  mentioned  as  homes  of  the  disease.  Bruce 
Perry  and  Fraser  Roberts  [11]  found  a significant  association 
between  the  density  of  persons  per  room  in  Bristol  and  the 
incidence  of  rheumatic  heart  disease.  Daniel  [14],  also  in 
Bristol,  revealed  a significant  association  ■with  differences  in 
family  income  and  significant  variations  with  the  number 
of  rooms  used  by  each  family  divided  by  the  number  of 
persons  in  the  family.  Miller  [9]  concluded  that  there  was 
a higher  incidence  in  the  artisan  class  than  in  the  poorest 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  453 
group,  but  this  view  is  not  supported  by  Morris  and  Titmuss 
[1].  Of  the  factors  operating  within  the  general  framework 
of  poverty,  damp  houses  have  often  been  suspect,  and 
Daniel  found  slight  suggestive  evidence  of  the  effect  of 
living  or  sleeping  in  basements.  Crowding,  with  increased 
liability  to  droplet  infections,  would  seem  to  be  more 
definitely  incriminated. 

Nutritional  deficiency,  with  impaired  resistance  to  infec- 
tion, has  naturally  been  suggested  as  a factor  dependent 
upon  low  economic  status.  Warner  and  Winterton  [17J 
discovered  no  appreciable  signs  of  under-nourishment  in 
rheumatic  children  as  compared  with  a control  group,  but 
considered  that  animal  protein  and  the  dairy  product 
components  of  the  dietary  in  the  social  groups  studied 
were  lower  than  they  should  be.  Coburn  and  Moore  [18] 
were  more  strongly  inclined  to  incriminate  sub-standard 
diets,  but  not  a deficiency  of  any  one  dietary  factor. 
Holland  Clarke  [13],  describing  his  Dublin  experience,  was 
more  impressed  in  all  working-class  occupational  grades  by 
the  factor  of  bad  housing  and  sleeping  accommodation  than 
by  that  of  low  family  budgets.  Green  [19],  on  the  other  hand, 
in  on  epidemic  of  rheumatic  fever  among  naval  apprentices, 
found  a much  higher  incidence  among  the  less-favoured 
Tyneside  boys  than  among  boys  from  other  parts  of  the 
country  who  were  similarly  exposed. 

Before  the  other  influences  associated  with  poverty  are 
too  strongly  incriminated,  the  effects  of  crowding  without 
poverty  or  nutritional  deficiency  should  be  considered.  If 
droplet  infection  with  the  streptococcus  is,  os  is  now  widely 
accepted,  an  important  specific  factor,  local  epidemics 
might  he  expected  to  occur  among  boys  or  girls  or  young 
adults  well  cared  for  in  other  respects  but  subjected  to 
overcrowding  through  defective  dormitory  spacing.  Such 
local  epidemics  have  occurred  in  training  ships  and  in 
barracks,  where  other  influences,  whether  in  respect  of 
nutrition  or  open-air  exercise  and  recreation,  were  not 
unfavourable.  Dudley  [20]  gave  an  account  of  the  high 
incidence  of  sore  throats  and  rheumatic  attacks  in  training 
ships  and  establislunents,  but  was  inclined  to  blame  damp 


454  THE  SOCIAL  PATHOLOGY  Or  RHEUMATIC  FETOR 
nnd  cliill  more  than  crowding.  Green  [19]  described  similar 
outbreaks  among  naval  apprentices  living  at  close  quarters 
and  partly  in  hutments,  although  muddy  approaches  and 
wet  feet  may  here  have  been  a factor.  Glover  [21]  found 
that  the  incidence  of  acute  rheumatism  among  army 
recruits  in  barracks  was  directly  correlated  with  over- 
crowding. Fcasby  [22]  has  discussed  rheumatic  fever  in 
relation  to  streptococcal  infections  in  the  Canadian  Army 
during  the  war,  and  Ilare  [23],  accepting  the  association, 
has  reviewed  methods  of  prevention  of  streptococcal  epi- 
demics and  rheumatic  fever  in  the  armed  forces.  In  the 
U.S.A.,  streptococcal  and  rheumatic  fever  outbreaks  among 
naval  and  military’  personnel  have  also  presented  a con- 
siderable problem  during  the  war.  Crowding  in  barracks  or 
hutments  of  boys  or  men  still  at  a susceptible  age  would 
seem — as  in  the  case  of  cerebrospinal  meningitis  [21] — to  be 
the  likely  common  factor  in  the  various  outbreaks  described. 
If  damp  and  chill  arc  potent  factors,  why  was  rheumatic 
fever  so  rare  in  young  soldiers  during  the  trench  warfare  of 
1914-18  ? 

Although  rheumatic  fever  has  had  a low  incidence  in 
British  public  schools,  Bradley  [24]  reported  two  outbreaks 
of  streptococcal  sore  throat  at  a well-to-do  public  school 
housing  340  boys.  There  were  twenty-nine  attacks  of  acute 
rheumatism,  affecting  25  boys,  and  among  these  20  cases 
of  carditis.  He  stated  that  hygienic  arrangements  were 
satisfactory,  ‘except  for  some  overcrowding  and  the  fact 
that  the  boys  live  in  one  building  and  not  in  separate 
houses’.  Here  such  factors  as  damp  or  chill  nnd  present  or 
antecedent  dietary  shortage  could  be  reasonably  excluded. 

Social  studies  of  individual  cases  of  rheumatic  fever  in 
children — and  here  the  hospital  or  municipal  almoner  as 
medical  social  worker  has  an  important  part  to  play — will 
frequently  reveal  the  adverse  conditions  in  which  a child 
has  been  living  before  the  first  or  subsequent  attacks. 
Home  visits  can  also  provide  other  important  evidence 
bearing  upon  the  varied  role  of  a common  infective  agent 
in  a domestic  epidemic  [25].  The  domestic  epidemic  of 
streptococcal  infection  is,  indeed,  worthy  of  much  closer 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  -155 
study.  In  two  cases  of  rheumatic  carditis  in  children  which 
I employed  recently  as  texts  for  a socio-medical  student 
conference,  the  family  budgets  were  considered  adequate, 
but  the  bedroom  accommodation  was  inadequate.  In  1937 
I saw  the  following  case  with  W.  H.  Bra  die}',  the  account  of 
which  he  included  later  in  a paper  on  the  spread  of  strepto- 
coccal disease  [25]: 

‘On  March  2,  1037,  Gwendoline,  daughter  of  a farm  labourer  in 
an  English  village,  went  to  bed  with  a bad  cold,  and  felt  HI  until 
Starch  8.  On  March  7,  however,  she  got  up  because  her  mother  was 
delivered  of  a baby — the  eighth  in  the  family.  She  helped  nurse  her 
mother,  who,  on  March  10,  became  suddenly  ill  with  puerperal  fever, 
associated  with  a scarlatiniform  rash,  from  which  she  eventually 
died.  Fourteen  days  after  the  onset  of  the  mother's  illness,  the  father 
liad  “ influenza",  and  Evelyn,  aged  4,  contracted  a severe  cold  2 days 
later,  while  5 days  later,  on  April  1,  Gladys,  aged  17,  had  a cold,  and 
on  April  7,  Fred,  aged  14,  contracted  "influenza".  On  April  6, 
Gwendoline  was  troubled  with  pains  in  her  lower  abdomen,  which 
persisted  for  3 days.  She  was  vaguely  unwell  until  April  0,  when  her 
illness  declared  itself  as  typical  rheumatic  fever.  Type  15/17  strep- 
tococci were  recovered  from  the  throats  of  4 of  these  patients,  but 
were  absent  from  the  mother’s  throat.  A pure  culture  of  this  organ- 
ism was,  however,  obtained  from  the  pus  in  a pelvic  abscess  subse- 
quently operated  upon.’ 

Without  this  specific  domestic  investigation  the  child  and 
her  mother  might  have  been  ndmitted  to  the  same  hospitnl 
and  clinically  and  pathologically  investigated  there  in  the 
usual  manner  without  any  connexion  being  established 
between  the  two  cases,  and  without  any  light  being  thrown 
upon  those  adverse  social  influences  in  the  absence  of  which 
both  of  them  might  have  remained  well.  The  family,  ns  the 
smallest  social  unit,  is  ns  worthy  of  investigation  ns  are  the 
larger  types  of  population.  It  can  also  be  more  intimately 
and  humanely  studied,  and  with  reference  to  psychological 
and  genetic  as  well  as  to  economic  and  other  influences. 


The  Extension  of  Social  Inquiry 
While  the  conditions  of  life  of  the  working-class  popu- 
lation may  to-day  be  accepted  ns  a main  actiologicnl 
factor  in  rheumatic  fever  and  carditis,  it  is — as  has  been 


45G  TUE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FETOR 
suggested — not  enough  to  blame  poverty  without  consider- 
ing the  influences  within  the  framework  of  poverty  which 
are  particularly  responsible.  Here  we  must  confess  that  we 
are  badly  in  need  of  fuller  information  bearing  upon  urban, 
rural,  institutional,  and  domestic  epidemiology.  Morbidity 
must  supplement  mortality  studies.  How  can  the  informa- 
tion be  collected  ? Many  writers  have  advocated  notifica- 
tion, and  it  has  been  locally  operated.  I confess  that  its 
general  enforcement  now  seems  to  me  to  have  become  an 
urgent  necessity.  Parkinson’s  [2]  recent  insistence  that 
‘compulsory  notification  of  rheumatic  fever  is  essential  to 
any  effort  to  deal  with  it  on  a national  scale  * will  probably 
be  widely  endorsed.  Without  it,  we  can  learn  little  more  of 
the  secular  trend  of  the  disease  or  of  regional  or  seasonal 
fluctuations.  Without  it,  local  health  officers  are  not  in  a 
position  to  conduct  planned  surveys;  to  inquire  into  the 
domestic  and  other  conditions  obtaining  in  individual 
cases;  to  consider  under  the  effects  of  crowding  the  respect- 
ive contributions  of  restricted  space,  damp,  poor  ventilation 
and  lighting  and,  possibly,  blanket-dust ; or  to  pursue  over 
a period  of  years  the  results  of  such  experiments  of  op- 
portunity as  are  made  possible  at  a time  of  rehousing. 
How  far  will  the  trend  of  rheumatic  fever  in  a city  with  a 
high  incidence  be  influenced  by  the  gradual  transfer  of 
ill-housed  populations  to  new  estates  ? How  far  are  secon- 
dary' attack-rates  in  individuals  affected  by  improved 
sleeping  accommodation  and  better-built  houses  ? To  what 
extent  may  day-school,  as  distinct  from  domestic,  epidemics 
of  sore  throat  have  an  effect  on  the  rheumatic  fever  rate  ? 
Should  the  institutional  epidemic  be  related  to  heightened 
bacterial  virulence,  or,  more  simply,  to  heightened  atmo- 
spheric concentration  of  bacteria  with  increased  exposure 
risks — in  fact,  to  bacterial  as  well  as  human  ‘crowding’? 
Here  are  same  questions  awaiting  answer. 

In  discussing  social  pathology,  it  would  be  outside  my 
province  to  consider  how  important  to  the  individual  case 
immediate  investigations  of  home  conditions  on  notifica- 
tion, earlier  removal  to  hospital,  and  subsequent  domiciliary 
visits  on  discharge  from  hospital,  might  be.  It  is,  however. 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  457 
reasonable  to  suggest  that  organized  domestic  studies 
might  make  important  contributions  to  the  better  under- 
standing of  the  natural  history  of  the  disease  both  in 
individuals  and  in  the  community,  and  thereby,  in  due 
course,  to  prevention  and  treatment. 

Notification 

There  is  no  sound  reason  why  notification  should  be 
reserved  for  the  more  obviously  communicable  diseases. 
If  it  can  be  shown  to  be  in  the  general  interests  of  the  public 
health  and  can,  sooner  or  later,  assist  the  prevention  of  a 
common,  costly,  and  crippling  disease,  it  is  obviously  sound 
policy,  whether  from  the  point  of  view  of  hygiene,  humanity, 
or  economics.  We  must  not,  however,  overlook  certain 
difficulties  which  might  be  connected  with  notification. 
The  more  obvious  difficulties  and  how  they  might  be  met 
are  briefly  considered  hereunder: 

1.  The  diagnosis  of  rheumatic  fever  is  often  much  more 
difficult  than  that  of  any  of  the  common  exanthemata, 
but  perhaps  not  greatly  more  so  than  that  of  pulmonary 
tuberculosis  in  its  early  stages.  As  in  the  case  of  the  last- 
named  disease,  consultant  and  other  facilities  are  likely,  in 
the  near  future,  to  become  available  in  all  cases  of  doubt. 

2.  Unlike  the  common  exanthemata,  rheumatic  fever  is 
often  recurrent.  Should  secondary  attacks  be  reported  ? 
YVhat  should  be  the  criteria  for  notifying  primary  and 
secondary  attacks?  Should  a rheumatic  heart  lesion  dis- 
covered for  the  first  time  in  a child  or  adolescent  in  the 
absence  of  recent  activation  be  notified?  It  might  be 
stipulated  that  for  purposes  of  central  registration,  all  cases 
of  juvenile  rheumatism  and  chorea,  and  of  acute  carditis 
and  valvular  disease  in  young  persons,  believed  to  be  of 
rheumatic  origin  and  seen  for  the  first  time,  should  be 
notified  locally  and  centrally;  while  nil  secondary  attacks 
should  be  locally  notified  in  order  to  ensure  the  fullest 
possible  co-operation  between  practitioner,  local  health 
authority  and  consultant,  and  the  full  use  of  special  clinics 
or  social  services.  Old-established  rheumatic  heart  disease, 
not  recently  reactivated,  and  seen  for  late  cardiac  symptoms 


458  THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER 
or  discovered  in  the  course  of  a general  examination,  should 
not  be  notified. 


Summary 

If  social  medicine,  in  its  broadest  connotation,  is  to  be 
given  its  fullest  practical  opportunity,  it  must  be  scientifi- 
cally supported  by  a sound  pathology.  The  social  pathology 
of  a disease  is  largely  dependent  upon  reliable  clinical, 
statistical,  and  social  data,  and  especially  upon  morbidity 
and  mortality  figures  and  their  correlations  with  measurable 
social  influences. 

In  tuberculosis,  while  we  are  all  agreed  that  mortality 
studies  alone  are  not  enough,  we  have  been  slow  to  make 
full  use  of  our  material  bearing  upon  morbidity.  Benefiting 
by  our  experience  and  omissions  in  respect  of  tuberculosis, 
it  should  be  possible  to  utilize  notifications  of  rheumatic 
fever  and  carditis  more  effectively  from  the  moment  of 
their  introduction,  and  thereby  more  expeditiously  to 
advance  our  understanding  of  causes  and  prevention.  In 
support  of  statistical  analyses  of  official  returns,  planned 
socio-medical  surveys  in  large  cities,  intimate  domestic 
studies,  and  long-term  social  experiments  in  populations 
destined  for  rehousing,  should  also  have  a part  to  play. 
The  disease  has  been  very  closely  studied  in  the  individual — • 
living  and  dead.  It  should  now  be  our  aim  to  maintain  a 
continuing  study  of  the  living  disease  in  the  community, 
and  in  the  process — valuable  though  they  must  remain — • 
to  rely  less  exclusively  upon  the  methods  of  the  social 
post-mortem  examination. 

Conclusions 

Poor  social  circumstance,  and  especially  the  conditions 
accompanying  working-class  life  in  large  cities,  have  been 
established  in  this  country  and  elsewhere  as  having  out- 
standing aetiological  importance  in  rheumatic  fever. 

Of  the  factors  operating  within  the  general  framework 
of  poverty,  overcrowding  is  probably  the  most  potent. 
The  fact  that  outbreaks  of  streptococcal  sore  throat  and 
rheumatic  fever  occur  in  residential  schools,  training  ships. 


THE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER  459 
and  barracks,  where  general  hygiene,  nutrition,  and  medical 
supervision  arc  usually  good,  supports  this  view.  Crowding 
itself,  however,  is  a further  subject  for  study,  for  limitation 
of  cubic  space  is  not  the  sole  factor  at  work.  Defective 
ventilation  and  lighting,  and  dust,  may  all  help  to  maintain 
too  high  a concentration  of  noxious  bacteria.  Disturbed  sleep 
and  lack  of  opportunity  for  open-air  play  may  impair 
resistance  to  infection. 

Actions  prompted  by  general  aetiological  considerations 
should  not  be  postponed  until  specific  aetiologies  are 
clarified. 

Compulsory  notification  of  rheumatic  fever  would  greatly 
assist  those  epidemiological  and  aetiological  studies  upon 
which  the  further  development  of  preventive  action  must 
be  based. 


REFERENCES 

1.  Morris,  J.  N,  and  Tmitrss,  R.  M.  (1012):  ‘Epidemiology  of 

Juvenile  Rheumatism’,  Lancet,  ii.  50. 

2.  Parkinson,  j.  (1015):  ‘Rheumatic  Fever  and  Heart  Disease’ 

(Harvcian  Oration),  Lancet,  ii.  G57. 

3.  Bach,  F„  Hill,  N.  G.,  Preston,  T.  \Vm  and  Thornton,  C,  E. 

(1039):  ‘Juvenile  Rheumatism  in  London’,  The  Jtheum.  I)is., 
i.  210. 

4.  Barclay,  P.  E.,  and  King-Lewis,  F.  L.  (1015):  ‘Prophylactic 

Use  of  Sulphonamidcs  in  Rheumatic  Fever’,  Lancet,  Ii.  751. 

5.  Pickles,  \V.  N.  (1043):  *A  Rheumatic  Family  % Lancet,  ii.  211. 
0.  Read,  F.  E.  M„  Ciocco,  A.,  and  Taussjg,  II.  B.  (1038):  ‘The 

Frequency  of  Rheumatic  Manifestations  among  the  Siblings, 
Parents,  Uncles,  Aunts,  and  Grandparents  of  Rheumatic  and 
Control  Patients',  Amer.  Joum.  of  Hygiene,  xxvii.  710. 

7.  YotjNtj,  M.  (1025):  ‘The  Geographical  Distribution  of  Heart 

Disease  in  England  and  Wales’,  Lancet,  ii.  500. 

8.  Young,  M.  (1927):  ‘Some  Observations  on  the  Mortality  from 

Rheumatic  Fever  nnd  Heart  Disease’,  Lancet , ii.  10C9. 

9.  Miller,  R.  (1012);  ‘Juvenile  Rheumatism;  Its  Problems’, 

Ixincet,  H.  503. 

10.  Medical  Research  Council  (1927):  ‘Social  Conditions  nnd 

Acute  Rheumatism*,  Special  Report  Series,  No.  11 1. 

11.  Bruce-Peury,  C.,  and  Fraser  Roberts,  J.  A.  (1037):  ‘A  Study 

of  the  Variability  in  the  Incidence  of  Rheumatic  Heart  Disease 
within  the  City  of  Bristol’,  I3.MJ.  ii.  151. 


4G0  TIIE  SOCIAL  PATHOLOGY  OF  RHEUMATIC  FEVER 

12.  Poynton,  F.  J.  (1038):  ‘Juvenile  Rheumatism — The  Social 

Aspect’,  Proceedings  of  the  International  Congress  on  Rheuma- 
tism and  Hydrology,  p.  171. 

13.  Holland  Clarke,  I*.  J.  (10  SO):  ‘The  Clinical  and  Public  Health 

Aspects  of  Juvenile  Rheumatism  in  Dublin’,  Irish  Joum.  of 
Med.  Science,  clxxi.  07. 

14.  Daniel,  G.  II.  (1012):  ‘Social  and  Economic  Conditions  in  the 

Incidence  of  nheumatic  neaft  Disease*,  Joum.  Royal  Slat. 
Soc.  cv.  107. 

15.  Donovan,  G.  E.  (1044):  ‘Some  Aspects  of  Cardiovascular 

Disease  with  Special  Reference  to  Public  Health’,  Public 
Health,  Ivii.  85. 

10.  Morris,  J.  N.,  and  Titmuss,  R.  M.  (1014):  'Health  and  Social 
Change:  The  Recent  History  of  Rheumatic  Heart  Disease’, 
The  Mtd.  Officer,  Ixxii.  CO,  77,  and  85. 

17.  'Warner,  E.  C.,  and  Winter-ton,  F.  C.  (1035):  ‘A  Dietetic  Study 

of  Cases  or  Juvenile  Rheumatic  Disease’,  Quart.  Joum.  Med., 
Oxford,  xxviii.  227. 

18.  ConciiN,  A.  F.,  and  Moore,  L.  V.  (1013):  ‘Nutrition  as  a Condi- 

tioning Factor  in  the  Rheumatic  State’,  Amer.  Joum.  of  His. 
of  Children,  Ixv.  744. 

10.  Green,  C.  A.  (1042) : ‘Epidemiology  of  Haemolytic  Streptococcal 
Infections  in  Relation  to  Acute  Rheumatism’,  Joum.  of 
Hygiene,  Cambridge,  xlii.  305. 

20.  Dudley,  S.  F.  (1020):  ‘The  Spread  of  Droplet  Infection  in  Semi- 

Isolated  Communities’,  M.R.C.,  Special  Report  Series,  No.  111. 

21.  Glover,  J.  A.  (1030):  Milroy  Lecture  on  ‘The  Incidence  of 

Rheumatic  Diseases  Lancet,  i.  400. 

22.  Feasby,  W.  R.  (1044):  ‘Rheumatic  Fever  in  the  Canadian 

Army’,  War  Medicine,  vi.  130. 

23.  Hare,  H.  (1043):  Canadian  Med.  Assoc.  Joum.  xlviii.  110. 

24.  Bradley,  W.  H.  (1032):  ‘Epidemic  Acute  Rheumatism  in  a 

Public  School*,  Quart.  Joum.  Med.,  Oxford,  xxv.  70. 

25.  Bradley,  W.  H.  (1038):  ‘The  Spread  of  Streptococcal  Disease’, 

BJlf-7.  ii.  733. 


XXXVII 

THE  HIPPOCRATIC  IDEAL1 


Tiie  sources  of  inspiration  in  medicine  and  the  medical 
sciences  are  many  and  varied.  There  are  advantages  at  all 
times,  but  especially  in  an  age  of  swift  material  progress, 
stem  competition,  and  perplexing  prospects,  in  pausing 
occasionally  to  consider  the  motives  which  prompt  us  and 
the  beliefs  which  sustain  us  in  our  choice  of  career  and  in 
our  daily  work.  As  a profession  closely  concerned  with  the 
health  and  affairs  of  the  individual  and  the  community  wc 
are  exposed  not  a little  to  criticisms  both  of  a private  and  a 
public  kind,  and,  partly  at  the  direction  of  the  modern  press, 
which  thrives  on  scandal  and  open  dissection  of  human 
frailties,  we  have  come,  perhaps,  to  incur  a larger  measure 
of  censure  than  was  allotted  to  earlier  generations  of  doctors. 
Whether  the  criticisms  wc  encounter  have  relation  to  our 
manners  and  peculiarities,  our  education,  our  attitude  to 
unorthodox  therapy,  our  jealousies,  our  technical  failures, 
or  to  other  defects  in  our  constitutions  and  our  actions,  and 
unjust  though  many  of  them  may  be,  we  would  be  foolish 
and  conceited  to  suppose  that  none  of  them  arc  ever  well 
grounded.  Wc  are  human  and  fallible.  Our  problems  both 
of  science  and  of  practice  arc  far  too  difficult  for  us  to  adopt 
on  attitude  of  complacency  or  superiority. 

Science  forges  ahead,  often  to  the  embarrassment  of 
practice ; times  and  habits  change  and  ethics  suffer.  At  the 
present  time  there  are,  I would  submit,  many  cogent 
reasons  for  a review  of  motives  and  beliefs  and  for  a dis- 
cussion of  those  ideals  without  which  no  body  of  scientists 
or  humanists  can  profitably  proceed.  The  beginning  of  a 
new  session,  the  meeting  of  an  old  and  honoured  society 
commemorative  in  name  and  aims  of  the  work  of  a great 
man,  and  the  precincts  of  one  of  the  oldest  and  finest 

* An  address  delivered  to  the  Abemethian  Sodety,  St.  Bartholomew's 
Hospital,  13  November  1034  (Lancet,  1031,  II.  12C3). 


402  THE  HIPPOCRATIC  IDEAL 

hospitals  and  medical  schools  in  the  world,  provide  an 

appropriate  occasion  and  place  for  such  a review. 

I have  said  that  the  sources  of  inspiration  in  medicine  are 
many  and  varied.  Uncritically,  perhaps,  for  our  life  is  full 
and  exacting  and  we  have  small  time  for  personal  analysis, 
we  all  of  us  perceive  that  our  steps  have  been  directed  and 
our  endeavours  supported  on  the  one  hand  by  the  humane 
and  on  the  other  by  the  scientific  interests  of  medical  work, 
and,  even  through  times  of  tedium  or  disappointment,  and 
while  recognizing  that  our  labour  is  also  our  livelihood, 
most  of  us  continue  to  be  actuated  by  these  interests. 

The  inspiration  of  our  teachers  and  the  traditions  of  our 
school,  of  contemporary  discoveries  such  as  those  of  Banting 
and  of  Minot,  of  the  journals  and  the  monographs,  and,  by 
no  means  least,  of  the  medical  society — upon  the  moral  and 
practical  value  of  which  Osier  was  so  rightly  insistent — all 
these  lend  their  quota.  Too  few  of  us  are  tempted  to  explore 
the  attractive  field  of  medical  history,  and  yet  not  one  of 
us  goes  forth  into  the  world  without  some  consciousness 
of  his  debt  to  those  old  masters  who  are  more  to  the  eras  of 
medicine  than  kings  and  governments  have  been  to  the 
eras  of  social  and  political  history.  The  experiment  of  your 
own  immortal  Harvey ; the  clinical  method  of  Sydenham; 
the  work  of  the  physician-pathologists  Bright,  Addison, 
Hodgkin,  and  Wilks  in  my  own  school ; Jenner’s  discovery'; 
the  contributions  of  Pasteur  and  Lister;  and  the  brilliant 
advances  due  to  the  physiologists  in  the  last  century,  have 
provided  us  with  a wealth  of  inspiration  upon  which  each 
of  us  must  continue  to  draw  through  life  in  greater  or  less 
degree. 

But  it  is  my  purpose  to  go  back  to  a far  earlier  period  for 
a source  of  inspiration  which,  through  many  centuries,  was 
accounted  the  most  profound  and  inexhaustible  of  all,  and  to 
show  you  that,  with  all  our  multitudinous  discoveries  and 
fresh  forms  of  knowledge,  we  can  still  find  in  the  work  and 
wisdom  of  Hippocrates,  and  of  those  who  composed  the 
Hippocratic  school,  a method,  a science,  an  art  of  practice, 
and  a code  of  professional  conduct  upon  which,  as  supplying 
a foundation  and  an  ideal,  no  subsequent  generation  has 


THE  HIPPOCRATIC  IDEAL  403 

been  able  to  improve.  I shall  hope  to  persuade  you  that 
occasional  readings  of  Hippocrates  are  by  no  means  out  of 
date  or  a waste  of  time ; to  stir  in  those  of  you  who  do  not 
already  possess  it  a veneration  for  one  of  the  noblest  figures 
in  that  rich  and  lovely  age  of  Grecian  culture;  and  to  remind 
you  that,  lacking  all  the  benefits  of  physiology  and  patho- 
logy,  Hippocrates  has  nevertheless  left  us  lessons  in  clinical 
method  and  record,  observations  on  prognosis,  a rational 
therapeutic  system,  and,  in  addition,  an  outline  of  medical 
ethics,  from  which  we  can  derive  instruction  and  correction 
to  this  day. 

In  case  you  should  doubt  the  reasonableness  of  an  appeal 
to  such  ancient  doctrine  I need  but  remind  you  that  philoso- 
phers in  all  subsequent  ages  have  found  the  chief  fountain 
of  their  inspiration  in  the  writings  of  men  who  were  the 
near  contemporaries  of  Hippocrates,  and  that  just  as  the 
Socratic  Dialogues  of  Plato  have  remained  an  essential 
introduction  for  the  student  of  philosophy  and  the  Bible  an 
essential  introduction  for  the  student  of  Christian  morals, 
so  might  the  Hippocratic  Collection,  or  at  least  selected 
readings  therefrom,  serve  as  an  introduction  for  the  student 
of  the  medical  arts  and  sciences.  It  is  n pity  that  the  prac- 
tical demands  of  medical  education  and  the  incessant 
developments  and  discoveries  of  the  clinical  and  ancillary 
sciences  should,  by  degrees,  but  so  largely,  have  excluded  the 
desire  for  contact  with  early  authority.  It  is  our  loss,  too, 
that  no  individual  to-day  is  so  equipped  intellectually  as  to 
be  able  again  to  stand  aside  and  take  the  general  view  of 
medicine  in  its  entirety,  to  correlate  its  problems,  to  balance 
its  science  with  its  art,  to  perceive  and  assess  the  compo- 
nents which  make  up  the  intricate  ‘whole’  presented  to  us  in 
the  shape  of  a ‘disease*  or  a ‘sick  man*.  We  have  become, 
inevitably,  too  knowledgeable  and  too  specialized.  In  the 
endeavour  to  think  sufficiently  anatomically  or  physiologi- 
cally j sufficiently  in  terms  of  infection  and  the  immunity- 
response;  to  assess  the  constitutional,  the  environmental, 
and  tlie  psychological  factors  in  the  individual  case — or, 
in  other  words,  to  bring  together  our  too  disjointed  know- 
ledge for  the  solution  of  the  individual  puzzle — we  commonly 


404  THE  IIIPPOCriATIC  IDEAL 

fail  or  achieve  but  a partial  success,  and  in  our  treatment 
we  often  interfere  too  much.  Sometimes,  I believe,  Hippo- 
crates, with  all  his  limitations,  would  have  succeeded  where 
we  fail  through  his  simple  habit  of  observing  and  noting  the 
facts  of  nature,  through  having  seen  the  same  things  before, 
through  his  recognition  of  disease  as  a natural  process  rather 
than  an  'abnormality'  (which  after  all  is  but  a small  ad- 
vance on  the  old  idea  of  demonic  possession),  and  through 
his  clear  recognition  of  the  vis  medicalrix  naturae.  But  I 
move  ahead  of  my  theme. 


Lite  and  Work  of  Hippocrates 

Of  the  details  of  the  life  of  Hippocrates  little  is  known, 
but  we  have  evidence  that  he  flourished  in  the  fifth  century 
b.c.,  that  his  period  of  greatest  activity  was  in  the  latter 
half  of  that  century,  and  that  he  lived  to  a great  age. 

His  contemporaries  included  the  statesman  Pericles;  the 
poets  Aeschylus,  Sophocles,  and  Euripides;  Socrates  and 
Plato,  the  philosophers;  Herodotus  and  Thucydides,  the 
historians;  and  Phidias,  the  sculptor.  He  came  of  physi- 
cianly  stock,  and  probably  received  a part  of  his  early 
training  in  the  temples  of  Health  from  his  own  father.  The 
school  which  he  founded  was  in  the  little  island  of  Cos  in  the 
Aegean  Sea.  In  the  market-place  of  the  chief  town  of  Cos 
there  still  stands  a very  aged  plane  tree  which  is  reputed  to 
have  flourished  in  his  day,  and  in  the  shade  of  which  he  is 
believed  to  have  taught.  Expert  opinion  has  pronounced  it 
possible  for  the  tree  to  have  endured  such  longevity.  In 
his  later  years  Hippocrates  travelled  much.  His  advice  was 
in  gxeat  demand,  and  he  won  in  bis  lifetime  a degree  of 
respect  and  veneration  foreshadowing  and  in  full  keeping 
with  his  later  fame. 

The  Hippocratic  Collection  consists  of  a number  of 
writings  on  medical  and  allied  topics,  some  of  which  are 
ascribed  directly  to  Hippocrates  himself,  some  (which  may 
yet  be  regarded  as  genuine  products  of  his  school)  to  his 
disciples,  and  others  which  are  now  accounted  as  spurious 
and  of  later  date.  Among  the  more  noteworthy  of  these 


THE  HIPPOCRATIC  IDEAL  405 

writings  are  the  following:  Epidemics,  I and  HI;  Airs, 
Waters,  Places;  The  Aphorisms ; Prognostic;  Regimen  in 
Health ; Regimen  in  Acute  Disease;  The  Oath;  1 Founds  of 
the  Head;  Fractures;  Joints;  The  Sacred  Disease. 

Of  his  work  and  practice  wc  may  assume  that  he  probably 
saw  and  advised  his  patients  and  taught  at  a temple  of 
Health  or  its  equivalent,  much  as  a modern  physician  might 
hold  his  clinic.  Probably  his  case  records  and  those  of  his 
assistants  were  accumulated  in  the  library  of  the  institution. 
Of  the  case-report  system  he  may  be  regarded  as  the  founder. 
We  have  no  doubt  from  his  vivid  descriptions  of  fever 
cases  in  The  Epidanics  that  he  also  visited  patients  in  their 
homes.  Occasionally  his  opinion  was  sought  by  public 
authorities  in  great  emergencies,  as  when  Athens  was 
afflicted  with  plague. 

The  Scientific  Ideal 

What  was  the  great  contribution  of  Hippocrates  to  the 
science  of  medicine?  The  advancement  of  the  biological 
sciences,  of  which  human  pathology  is  surely  not  the  least, 
has  depended  upon  the  combined  contributions  of  observa- 
tion and  experiment.  The  method  of  experiment  was  a late 
arrival  and,  although  there  were  experimenters  before  his 
time,  Harvey  may  be  regarded  as  its  first  outstanding  ex- 
ponent. Hippocrates  was  literally  the  founder  of  the  obser- 
vational method,  and  in  this  wc  may  claim  for  him  an  even 
greater  regard  than  that  implicit  in  his  familiar  title,  the 
Father  of  Medicine.  Wc  have  to  imagine  that  before  his 
day  medicine  was  compounded  in  large  part  of  first  aid, 
quackery,  and  superstition,  and  that  even  physicians  of 
repute  relied  for  more  upon  tradition  and  speculation  than 
upon  recorded  fact.  Hippocrates  set  himself  steadfastly 
against  speculative  philosophies  and  quack  therapy,  and 
npplied  himself  to  the  task  of  accumulating  knowledge  of 
disease  and  of  man  in  disease  by  accurately  recording  what 
his  own  senses  revealed  to  him.  The  method  was  extended 
to  the  whole  realm  of  natural  history  by  Aristotle,  but  it  is 
a matter  for  pride  that  a physician  (and  the  physician’s  work 

h h 


406  THE  HIPP 0 CRATIC  IDEAL 

bears  close  similarities  with  that  of  the  natural  historian)  was 
its  founder.  Prof.  J.  S.  Haldane,  in  his  Gifford  lectures  on 
The  Sciences  and  Philosophy  (1027-8),  writes  as  follows: 

‘Hippocrates  treated  the  unconscious  activities  of  life  as  natural 
processes.  He  claimed  the  right  to  interpret  them  in  accordance  with 
actual  observation,  regardless  of  superstition  and  of  the  intrusion  of 
philosophical  opinions  not  based  on  observation  of  them.  In  ob- 
serving Nature  just  as  she  appears  in  the  phenomena  of  life,  and 
basing  his  opinions  directly  on  the  observations,  he  founded  scientific 
medicine,  and  with  it,  os  it  seems  to  me,  scientific  biology.  The  co- 
ordinated activity  manifested  in  the  phenomena  of  life  was  regarded 
by  Hippocrates  as  nothing  more  than  a visible  and  tangible  manifesta- 
tion of  Nature.  . . . His  influence,  through  Aristotle  and  later  Greek 

thinkers  and  observers,  appears  to  have  been  a very  great  one It 

seems  to  me  that  the  attitude  of  Hippocrates  was,  and  Is,  the  only 
attitude  possible  in  scientific  biology.’ 

And  yet  how  constantly  has  specialization,  in  medicine 
and  biology,  led  to  a neglect  of  the  ‘co-ordinating  activity’ 
in  nature.  How  constantly  to-day  are  we  ‘side-tracked’ 
into  a contemplation  of  isolated  functions  and  ‘parts’  and 
a neglect  of  ‘wholes’.  Instead  of  man  wc  study  the  parts  of 
man;  instead  of  disease,  aspects  of  disease. 

Only  a reading  of  the  works  themselves  can  convey  a full 
idea  of  the  remarkable  powers  of  observation  possessed  by 
Hippocrates.  All  his  senses,  seeing,  heating,  feeling,  smell- 
ing, tasting,  must  have  been  assiduously  employed,  and  his 
deliberations,  based  on  his  sense-data,  were  illuminated  by 
the  clear  light  of  his  reason.  He  has  left  us  living  thumb-nail 
sketches  of  many  diseases,  including  mumps,  the  malarias, 
erysipelas  (mentioning  how  the  hair  falls  after  erysipelas  of 
the  scalp),  empyema,  puerperal  fever.  He  described  a 
number  of  valuable  signs  both  of  a general  and  a local  kind. 
The  Hippocratic  facies  of  impending  death  ‘with  sharp  nose 
and  hollow  eyes* ; Hippocratic  succussion.  in  pyo-pneumo- 
thorax ; ‘curved  nails’  ot,  as  we  should  call  them,  ‘clubbed 
fingers’  in  empyema;  splenic  enlargement  in  malaria; 
Cheyne-Stokes  breathing,  ‘respirations  rare  and  large  with 
long  intervals’,  to  use  his  own  words ; tetanus  after  wounds 
— are  all  depicted  in  his  records.  With  no  means  at  his 
disposal  for  minute  analysis  he  yet  gave  the  most  careful 


THE  HIPPOCRATIC  IDEAL  407 

attention  to  the  naked-eye  characters  of  the  excreta  and 
of  discharges. 

In  Precepts  he  advises  that  ‘one  must , . . occupy  oneself 
with  facts  persistently,  if  one  is  to  acquire  that  ready  and 
infallible  habit  which  we  call  “the  art  of  medicine”.  For  so 
to  do  will  bestow  a very  great  advantage  upon  sick  folk  and 
medical  practitioners.  Do  not  hesitate  to  inquire  of  laymen, 
if  thereby  there  seems  likely  to  result  any  improvement  in 
treatment/  The  most  scientifically  trained  among  us  are 
still  too  easily  tempted  to  toy  with  hypotheses  instead  of 
occupying  themselves  with  facts.  The  practitioner  remains 
unduly  reluctant  to  accept  help  or  suggestions  from  the 
layman.  In  Law  he  states  ‘there  arc  in  fact  two  things, 
science  and  opinion ; the  former  begets  knowledge,  the  latter 
ignorance’.  In  our  modern  medicine,  swayed  by  the  intricacy 
of  our  problems,  we  arc  still  sadly  prone  to  guesses  and 
‘opinions’  which  warp  the  truth-seeking  spirit.  In  Ancient 
Medicine  and  other  works  we  find  references  to  the  con- 
stitutional factor,  and  in  Airs,  Waters,  Places  to  the  environ- 
mental factors  in  disease. 


Prognosis 

Hippocrates  attached  a very  particular  importance  to 
prognosis. 

‘I  hold*,  he  said,  'that  it  is  an  excellent  thing  for  the  physician  to 
practise  forecasting.  For  if  lie  discover  and  declare  unaided  by  the 
side  of  his  patients  the  present,  the  past  and  the  future,  and  fill  in  the 
gaps  in  the  account  given  by  the  sict,  he  will  be  the  more  believed  to 
understand  the  cases,  so  that  men  will  confidently  entrust  themselves 
to  him  for  treatment.  Furthermore,  lie  will  carry  out  the  treatment 
best  if  lie  know  beforehand  from  the  present  symptoms  what  will 
take  place  later.’ 

Much  unnecessary  and  unwise  treatment,  both  medical 
and  surgical,  might  be  avoided  even  now  if  physicians  and 
surgeons,  less  wedded  to  medicines,  injections,  and  tech- 
niques, and  less  susceptible  to  the  impulse  ‘to  do  something* 
in  anxious  situations,  schooled  themselves  better  in  tliat 
knowledge  of  the  natural  course  and  eventualities  of  disease 
upon  which  all  sound  prognosis  and  treatment  depend. 

If  It  2 


468  THE  HIPPOCRATIC  IDEAL 

Hippocrates  knew  the  importance  of  many  prognostic 
signs  and  often  enough  their  limitations.  ‘If  a part  of  the 
white  appear  when  the  lids  are  closed,  should  the  cause  not 
be  diarrhoea  or  ■purging,  or  should  the  patient  not  be  in  the 
habit  of  so  sleeping,  it  is  an  unfavourable,  in  fact  a very 
deadly  symptom.’  Plucking  at  the  bed-clothes  in  fevers 
and  pneumonia  he  also  recognized  as  of  grave  import,  and 
also  grinding  the  teeth  in  fevers  'unless  it  has  been  a habit 
from  childhood'.  I would  ask  you  to  note  how  the  qualifica- 
tions which  I have  italicized  complete  the  accuracy  of  the 
observations.  The  advancement  of  diagnosis  and  prognosis 
has  depended  and  will  continue  to  depend  more  upon  exact 
clinical  observation  than  upon  any  other  single  factor. 

‘In  cases  of  ulcerated  tonsils’,  he  tells  us,  ‘the  formation 
of  a membrane  like  a spider’s  web  is  not  a good  sign*,  and 
‘ulcers  on  the  tonsils  that  spread  over  the  uvula  alter  the 
voice  of  those  who  recover’.  He  notices  that  injuries  or 
incisions  on  one  side  of  the  brain  produce  spasms  on  the 
other  side  of  the  body.  His  instructions  for  the  careful 
examination  of  head-wounds,  with  a note  on  the  importance 
of  discovering  if  the  bone  is  bare  and  of  distinguishing 
natural  sutures  from  traumatic  fissures,  are  as  useful  to-day 
as  when  they  were  written. 

Aphorisms 

His  Aphorisms,  many  of  them  beautifully  brief  and  to 
the  point,  are  clearly  the  crystallized  fruits  of  repeated 
observation  and  accumulated  experience.  Here  are  a few 
of  them: 

‘Old  men  endure  fasting  most  easily,  then  men  of  middle-age, 
youths  very  badly,  and  worst  of  all  children,  especially  those  of  a 
liveliness  greater  than  ordinary.’ 

‘When  sleep  puts  an  end  to  delirium  it  is  a good  sign.* 

‘Spontaneous  weariness  indicates  disease.’ 

‘In  every  disease  it  is  a good  sign  when  the  patient’s  intellect  is 
sound  and  he  enjoys  his  food.  The  opposite  is  a bad  sign.’ 

‘Those  who  are  constitutionally  very  fat  are  more  apt  to  die  quick]}' 
than  those  who  are  thin.’  (The  life  insurance  societies  know  this  well.) 

‘Pains  and  fevers  occur  when  pus  is  forming  rather  than  when  it 
has  been  formed.’ 

‘A  convulsion  supervening  upon  a wound  is  deadly.* 


THE  HIPPOCRATIC  IDEAL  4C9 

'Consumption  occurs  chiefly  between  the  ages  of  eighteen  and 
thirty-five.* 

* If  diarrhoea  attacks  a consumptive  patient  it  is  a fatal  symptom.’ 

‘Apoplexy  occurs  chiefly  between  the  ages  of  forty  and  sixty.* 

‘In  the  case  of  a person  afflicted  with  hiccough,  sneezing  coming 
on  removes  the  hiccough.* 

‘In  acute  diseases  chill  of  the  extremities  is  a bad  sign.’ 

4 Whenever  abscess  of  the  liver  is  treated  by  cautery  or  the  knife, 
if  the  pus  flow  pure  and  white,  the  patient  recovers,  for  in  such  cases 
the  pus  is  in  a membrane ; but  if  ft  flows  like  as  it  were  Ices  of  oil,  the 
patient  dies.* 

Was  he  contemplating  surgery  and  the  early  substitutes 
for  diathermy  in  malignant  growth  when  he  wrote : 'Those 
diseases  that  medicines  do  not  cure  arc  cured  by  the  knife. 
Those  that  the  knife  docs  not  cure  are  cured  by  fire.  Those 
that  lire  does  not  cure  must  be  considered  incurable*  ? 

The  examiners  may  require  us  to  know  the  calcium  con- 
tent of  the  blood  and  the  technique  of  the  Wasscrmnnn 
reaction.  The  aphorisms  are  more  useful  in  practice. 

In  describing  his  bedside  method  and  the  things  particu- 
larly to  be  observed  there  Hippocrates  wrote  as  follows: 

4 With  regard  to  diseases,  the  circumstances  from  which  we  form  a 
judgement  of  them  ore — by  attending  to  the  general  nature  of  all,  and 
the  peculiar  nature  of  each  Individual — to  the  disease,  the  patient  and 
the  applications — to  the  person  who  applies  them,  as  that  makes  a 
difference  for  better  or  worse — to  the  whole  constitution  of  the  season, 
and  particularly  to  the  state  of  the  heavens  and  the  nature  of  each 
country  ; to  the  patient’s  habits,  regimen  and  pursuits,  to  his  con- 
versation, manners,  taciturnity,  thoughts,  sleep,  or  absence  of  sleep, 
and  sometimes  his  dreams,  what  and  when  they  occur;  to  his  pick- 
ing and  scratching;  to  his  tears ; to  the  alvinc  discharges.  Urine,  sputa 
and  vomitings,  nnd  to  the  changes  of  diseases  from  one  to  another ; 
to  the  deposits  whether  of  a deadly  or  critical  character ; to  the  sweat, 
coldness,  rigor,  cough,  sneezing,  hiccough,  respiration,  eructation, 
flatulence,  whether  passed  silently  or  with  a noise;  to  haemorrhage 
and  haemorrhoids ; from  these  and  their  consequences  see  must  form 
our  judgement.* 

Could  we  desire  a more  concise  exhortation  to  attentive 
history- taking  and  clinical  observation? 

Ilis  philosophy  with  regard  to  disease  and  its  origins  is 
portrayed  in  the  beautiful  fragment  entitled  The  Sacred 
Disease,  the  name  given  to  epilepsy,  a disorder  considered 


470  THE  HIPPOCRATIC  IDEAL 

for  centuries  after  Hippocrates  to  be  an  evidence  of  demoniac 

possession: 

‘I  am  about*,  he aaj's,  ‘to  discuss  the  disease  called  “sacred”.  It 
is  not,  in  my  opinion,  any  more  divine  or  more  sacred  than  other 
diseases,  but  has  a natural  cause,  and  its  supposed  divine  origin  is  due 
to  men’s  inexperience,  and  to  their  vronder  at  its  peculiar  character.’ 
And  again:  ‘It  has  the  same  nature  as  other  diseases,  and  the  cause 
that  gives  rise  to  individual  diseases.  It  is  also  curable,  no  less  than 
other  Alnesses,  unless  by  long  lapse  of  time  it  be  so  ingrained  as  to  be 
more  powerful  than  the  remedies  that  are  applied.  Its  origin,  like 
that  of  other  diseases,  lies  in  heredity.’ 

In  the  same  work  he  discusses  the  brain  as  the  seat  of 
consciousness  and  the  emotions,  a conception  quite  un- 
familiar at  that  period,  when  the  heart  and  the  diaphragm 
were  commonly  held  to  be  the  scat  of  the  soul. 

Observation  and  Record 

The  importance  of  accurately  observing  and  recording 
facts;  of  studying  the  whole  event  and  all  attendant  cir- 
cumstances ; of  viewing  the  phenomena  of  disease  as  natural 
phenomena  and  not  as  due  to  malign  agencies  or,  as  we 
should  say,  ‘abnormalities’;  these,  in  brief,  are  the  main 
lessons  of  the  Hippocratic  creed.  To-day,  as  then,  the 
physician,  if  he  would  be  a good  healer,  must  first  be  a good 
natural  historian.  The  scientific  ideal  in  medicine  docs 
not  of  necessity  demand  intensive  study  of  minutiae,  pro- 
longed specialistic  inquiry,  or  training  or  discovery  by 
experiment  alone.  Rather  does  it  require  insistence  on 
truth,  correction  of  error,  an  understanding  of  the  methods 
whereby  truth  is  ascertained,  an  ability  to  sift  evidence, 
and  an  appreciation  of  ‘wholes’  and  of  those  co-ordinating 
activities  which  determine  the  nature  of  things,  and  without 
some  understanding  of  which  our  study  of  ‘parts’  may 
become  an  enfeebling  or  confusing  rather  than  an  enlighten- 
ing process.  Properly  used  and  weighed  bedside  experience 
can  point  the  way  to  the  goal  of  biological  truth  as  surely 
as  the  departmental  experience  of  the  laboratory. 

To  what  extent  does  modern  medical  education  help  us 
to  apply  the  Hippocratic  method  or  subserve  the  Hippo- 
cratic ideal  ? In  the  clinical  period  the  opportunity  is  there 


THE  HIPPOCRATIC  IDEAL  471 

for  all,  even  if  the  material  of  wards  and  out-patients  he 
too  limited,  lacking  much  that  the  life  of  practice  provides. 
We  have  also  the  guidance  of  our  teachers  and  the  stimulus 
of  contact  with  other  minds  pursuing  the  same  ends,  but 
we  must  confess  that  the  constant  increments  to  knowledge 
and  the  steady  arrival  of  new  diagnostic  tests  and  imple- 
ments encumber  us  with  difficulties,  and  in  some  degree 
hamper  both  the  use  of  the  unaided  senses  and  the  growth 
of  judgement.  Invaluable  though  our  accessory  methods  of 
inquiry  have  become,  wc  also  know  that  in  practice  many  of 
the  best  diagnoses  and  nearly  all  the  best  decisions  in  emer- 
gencies are  accomplished  without  radiological  or  laboratory 
aids.  In  the  prc-clinical  period,  although  a thorough  ground- 
ing in  chemistry,  physiology,  and  anatomy  is  an  obvious 
necessity,  it  seems  to  me  that  the  curriculum  provides  little 
scope  for  the  cultivation  of  ‘the  habit  of  observation’.  In  the 
dissecting-room  wc  train  our  hands  and  the  anatomical  sense, 
rediscovering  what  has  often  been  described,  but  wc  also 
exhaust  our  memories  with  names  of  parts,  and  wc  do  not 
learn  to  sec  new  and  vital  things  for  ourselves.  In  physio- 
logy, the  most  valuable  of  the  ancillary  subjects,  we  find 
our  introduction  to  the  experimental  method,  and  usefully 
train  the  mind  to  think  in  terms  of  function,  but  wc  tend  to 
lose  the  applications  of  such  knowledge  nnd  have  to  accept 
a number  of  doctrines  liable  themselves  to  flux  nnd  change, 
and  altogether  have  so  much  to  absorb  that  wc  commonly 
cease  to  inquire.  Much  of  this  basic  knowledge  in  anatomy 
and  physiology  is  essential;  much  of  the  detail  otherwise. 
We  use  the  microscope  and  the  test-tube,  nnd  we  must  know 
how  to  use  them,  but  little  is  done  to  exercise  the  unaided 
senses,  the  inquisitive  ‘look-about-you’  faculty,  the  sym- 
pathetic appreciation  of  vital  phenomena  as  shown  in 
human  feelings  and  actions,  or  to  train  the  mind  to  delect 
the  moods  nnd  passions  and  psychological  peculiarities  of 
other  minds.  Indeed,  for  the  first  three  years  of  the  medical 
curriculum,  the  observing  faculty,  which  is  so  sharp  in  the 
unencumbered  child,  so  necessary  in  the  naturalist  and  the 
physician,  and  which  was  developed  in  so  remarkable  a 
degree  by  Hippocrates,  is  not  only  not  encouraged,  but  to 


472  THE  IIIPPO  CI1ATIC  IDEAL 

some  extent  inhibited  by  educational  modes  which  seek  to 
harbour  the  scientific  spirit  with  a type  of  training  suitable 
for  the  student  of  physics  or  chemistry,  but  inappropriate 
for  the  student  of  man  in  health  nnd  disease.  On  entering 
the  wards  we  have  to  develop  a new  orientation  and  a new 
method,  and  in  the  process  most  of  wlmt  we  have  garnered  in 
the  prc-clinical  period,  and  even  much  of  what  was  useful 
therein,  rapidly  goes  by  the  board. 

One  of  my  own  teachers,  a great  surgeon,  clinician,  and 
pathologist,  the  late  Sir  Charters  Symonds,  urged  in  his 
Hunterian  Oration  fourteen  years  ago  tliat  clinical  oppor- 
tunities should  be  given  from  the  very  first.  ‘The  student  of 
medicine*,  he  said,  ‘throughout  his  life  must  be  sensible  of 
the  atmosphere  which  surrounds  the  sick-bcd.*  And  again: 
‘The  only  opportunity  the  student  of  medicine  has  for 
independent  observation  ...  is  in  the  clinical  field,  nnd  the 
sooner  he  is  brought  there  the  better.’  Many  of  us  share 
these  sentiments.  The  ward,  the  out-patient  clinic,  the 
consulting- room,  and  the  home  are  the  only  places  in  which 
we  can  learn  the  Hippocratic  method  at  first-hand. 

The  Therapeutic  Ideal 

Among  the  critics  of  Hippocrates,  nnd  even  this  great 
man  1ms  had  a few  detractors,  there  have  been  those  who 
objected  that  he  was  so  intent  upon  observing  disease  that 
he  neglected  his  patients.  Through  his  influence,  they 
would  aver,  other  physicians  in  other  ages  have  been  guilty 
of  scientific  callousness.  In  hospital  work  the  temptation 
to  be  interested  in  man’s  pathology  rather  than  in  man 
himself  is  one  which  some  find  difficult  to  resist,  but  that 
is  to  be  traced  rather  to  a narrow  curiosity  than  to  callous- 
ness, and  it  must  be  rare  indeed  for  it  to  lead  to  neglect. 

I have  found  nothing  in  my  own  reading  of  the  Hippocra- 
tic Collection  to  justify  the  criticism  as  directed  against  its 
author.  Recognizing  disease  processes  in  the  body  as  a con- 
test between  the  body  tissues  and  other  natural  agencies, 
and  aware  of  the  spontaneous  tendency  to  recovery  in 
the  great  majority  of  diseases  and  the  great  majority  of 
patients,  he  concluded  that  recover}'  from  disease,  just  like 


THE  HIPPOCRATIC  IDEAL  473 

disease  itself  or  death  from  disease,  was  a natural  phe- 
nomenon. ‘Nature’,  he  or  one  of  his  followers  said,  'is  the 
physician  of  diseases.'  Sydenham  expressed  himself  more 
strongly  when  he  declared  that  ‘To  imagine  Nature  in* 
capable  to  cure  diseases  is  blasphemy ; because  that  would 
be  imputing  imperfection  to  the  Deity,  who  has  made  a 
great  provision  for  the  preservation  of  animal  life’.  With 
our  more  intimate  understanding  of  pathology  we  continue 
to  support  this  doctrine.  We  continually  relieve  suffering 
by  surgery,  psychotherapy,  and  the  judicious  employment 
of  diet  and  drugs,  but,  if  we  except  the  knife  in  certain  types 
of  injury  and  local  disease,  a few  specific  chemicals  in  bac- 
terial or  protozoal  diseases,  the  substitution  therapies,  and 
one  or  two  life-saving  antitoxic  sera,  with  all  of  which  wc 
lend  a dramatic  assistance  to  nature,  wc  must  confess  that 
wc  arc  to  this  day  powerless  in  the  strict  sense  to  cure 
disease. 

We  have  ample  evidence  that  Hippocrates  did  not  with- 
hold, any  more  than  wc  do,  the  assistance  which  physician 
and  nurse  may  give  to  patients  to  enable  them  the  better  and 
the  more  speedily  and  comfortably  to  combat  their  maladies. 

In  surgery  he  insisted  on  cleanliness,  using  wine  for 
washing  wounds  and  urging  that  dryness  should  be  secured 
in  lacerated  wounds ; he  instructed  the  surgeon  to  keep  his 
nails  short ; he  trephined  for  certain  head  injuries ; he  taught 
methods  of  reducing  dislocations  which  wc  still  employ;  he 
recognized  the  therapeutic  value  of  rest,  and  of  hot  and 
cold  applications,  and  of  baths,  and  the  inadvisability  of 
prescribing  alcohol  in  head  injuries.  He  was  an  advocate 
of  barley  water  in  fevers  and  used  hydromcl  and  oxymel, 
giving  indications  for  each.  He  was  a good  psychologist,  as 
indeed  every  successful  physician  must  be.  Thus  he  speaks 
of  the  necessity  of  performing  actions  in  the  sick-room 
‘calmly  and  adroitly’,  of  giving  orders  ‘with  cheerfulness 
and  serenity’ ; but  sometimes  of ‘reproving  sharply  and  em- 
phatically’. He  advises  keeping  ‘a  watch  on  the  faults  of 
the  patients,  which  often  make  them  lie  about  the  taking 
of  things  prescribed*.  * One  must  not’,  he  says, ' be  anxious 
about  fixing  a fee.  For  I consider  such  a worry  to  be  harmful 


474  THE  nirrOCRATIC  IDEAL 

to  a troubled  patient,  particularly  if  the  disease  be  acute. . . . 
For,  in  heaven’s  name,  who  that  is  a brotherly  physician 
practises  with  such  hardness  of  heart  as  not  at  the  beginning 
to  conduct  a preliminary  examination  of  every  illness  and 
prescribe  what  will  help  towards  a cure,  to  heal  the  patient 
and  not  to  overlook  the  reward,  to  say  nothing  of  the  desire 
that  makes  a man  ready  to  learn?’ 

‘Loud  talking’,  we  are  reminded,  ‘is  painful.  Overwork 
calls  for  gentle  dissuasion.  A wooded  district  benefits.  * 

He  is  alive  to  the  disagreements  existing  among  physi- 
cians in  the  matter  of  therapeutic  beliefs,  and  of  the  discredit 
which  this  brings  them  in  the  minds  of  the  laity.  He  makes 
astute  observations  such  as  the  following:  ‘For  if  disease 
and  treatment  start  together,  the  disease  will  not  win  the 
race.’  I am  reminded  by  this  in  our  modem  medicine  of  the 
remarkable  effects  of  antitoxin  administered  early,  before 
the  spread  of  toxins,  in  diphtheria  and  infected  wounds, 
as  compared  with  the  much  more  dubious  influence  of  anti- 
streptococcal  and  antipneumococcal  sera,  which  can  seldom 
be  given  before  the  disease  is  established  and  declared. 
‘Do  not’,  he  says  ‘disturb  a patient  cither  during  or  just 
after  a crisis,  and  try  no  experiments,  neither  with  purges 
nor  with  other  irritants,  but  leave  them  alone.’  Regimen 
in  health  and  disease  receive  full  consideration,  but,  realizing 
the  variability  of  the  constitution  of  man  and  his  circum- 
stances, he  admits  that  ‘it  is  impossible  to  treat  of  the 
regimen  of  man  with  such  a nicety  as  to  make  the  exercises 
exactly  proportionate  to  the  amount  of  food’.  He  believes 
in  giving  responsibilities  to  dressers  and  clerks,  and  to  the 
patient. 

‘Let  one  of  your  pupils  be  left  in  charge,  to  carry  out  instructions 
without  unpleasantness,  and  to  administer  the  treatment.’  ‘The  art 
has  three  factors:  the  disease,  the  patient  and  the  physician.  The 
physician  is  the  servant  of  the  art.  The  patient  must  co-opcratc  with 
the  physician  in  combating  the  disease.* 

But  perhaps  the  greatest  therapeutic  principle  of  all  those 
which  the  Coan  school  has  left  to  us  is  this : ‘As  to  diseases, 
make  a habit  of  two  things — to  help,  or  at  least  to  do  no 
harm.’  As  experience  accumulates  many  of  us  must  reluc- 


THE  HIPPOCRATIC  IDEAL  475 

tantly  confess  that  we  see  a vast  deal  of  harm  in  practice 
due  to  injudicious  interference.  The  policy  of  ‘letting  well 
alone'  in  an.  improving  case,  even  though  improvement  be 
slight,  is  a sound  one,  but  often  ignored.  The  urge  ‘to  do 
something'  in  the  acute  or  anxious  ease,  even  though  it  be 
not  clear  what  that  ‘something’  should  be,  often  prevails, 
when  it  would  have  been  far  wiser  to  wait  and  watch. 
Against  the  countless  triumphs  of  surgery  we  have  to  set  a 
long  list  of  harmful  interferences,  especially  in  the  abdominal 
field.  The  more  potent  a treatment  is  for  good,  the  more 
potent  also  is  it  for  ill  when  misapplied.  It  is  important  to 
avoid  timidity  in  our  actions  or  a permanent  policy  of  laissez- 
faire,  but  in  being  bold  we  should  never  become  oblivious 
to  the  wise  restraint  of  thnt  injunction  to  ‘do  no  harm*. 

The  Ethical  Ideal 

If  there  be  present  need  for  a revision,  in  the  light  of 
early  teaching,  of  our  ideas  relating  to  the  science  and  art 
of  medicine,  the  occasion  is,  perhaps,  still  more  ripe  for  a 
revision  of  ethical  ideas.  The  War,  as  though  in  some  small 
compensation  for  vast  evil,  brought  benefits  to  medical  and 
surgical  knowledge,  hut  its  interruptions  have  in  some  degree 
been  damaging  to  the  old  ethical  standards  of  the  profession. 
The  former  friendly  relationship  between  doctor  and  doctor 
and  patient  and  doctor,  although  they  are  still  among  the 
happier  rewards  of  practice,  have  been  subjected  to  various 
strains,  and,  if  there  has  been  more  freedom  of  thought  and 
action,  this  has  sometimes  been  counterbalanced  by  a loss 
of  mutual  trust  and  understanding. 

I hear  occasional  complaints  from  older  men  that  appro- 
priation of  patients  by  newcomers,  criticisms  of  colleagues 
to  patients  and  by  patients,  and  uncorrccted  inconstancy 
among  patients  manifest  in  their  flittings  after  specialist 
and  unorthodox  opinion,  arc  much  more  common  than  in 
the  old  days.  Cloaked  advertisement,  ‘stunt’  treatments, 
and  commercial  methods  have  crept  in  insidiously  in  some 
quarters.  Jealousies  are  rife.  These  evils  arc  not  new,  but 
if  there  be  any  truth  in  the  impression  that  they  are  in- 
creasing it  is  time  that  a profession,  which  has  hitherto  mam- 


476  THE  HIPPOCRATIC  IDEAL 

tained  its  standards  at  a very  high  level,  should  immediately 

seek  to  set  its  house  in  order. 

The  rules  were  all  laid  down  between  two  and  three 
thousand  years  ago  in  the  Oath,  the  Precepts,  the  Decorum , 
Physician,  and  Laic  of  the  Hippocratic  Collection. 

In  the  Oath  the  physician  swears  among  other  things  that: 

‘Whatsoever  I shall  see  or  hear  in  the  course  of  my  profession,  as 
well  os  outside  my  profession  In  my  intercourse  with  men,  if  it  be 
what  should  not  be  published  abroad,  I will  never  divulge,  holding 
such  things  to  be  holy  secrets.’ 

We  cannot  too  often  remind  ourselves  of  the  importance 
of  professional  secrecy  or  too  closely  guard  our  tongues  from 
gossip. 

Of  the  physician  it  is  written  that: 

‘The  prudent  man  must  also  be  careful  of  certain  moral  considera- 
tions—not  only  to  be  silent  but  also  of  a great  regularity  of  life,  since 
thereby  his  reputation  wilt  be  greatly  enhanced ; he  must  be  a gentle- 
man in  character,  and  being  this  he  must  be  grave  and  kind  to  all.* 

‘Physicians  who  meet  in  consultation  must  never  quarrel,  or  jeer 
at  one  another.  For  I will  assert  upon  oath,  a physician's  reasoning 
should  never  be  jealous  of  another.  To  be  60  will  be  a sign  of  weak- 
ness. . . . You  must  also  avoid  adopting,  in  order  to  gain  n patient, 
luxurious  headgear  and  elaborate  perfume.  For  excess  of  strangeness 
will  win  you  ill-repute.  . . . Yet  I do  not  forbid  you  trying  to  please, 
for  it  is  not  unworthy  of  a physician’s  dignity. ...  A physician  docs 
not  violate  etiquette  even  if,  being  in  difliculties  on  occasion  over  a 
patient  and  in  the  dark  through  inexperience,  he  should  urge  the 
calling  in  of  others,  in  order  to  learn  by  consultation  the  truth  about 
the  case.’ 

Consideration  for  the  patient’s  pocket  could  scarcely 
be  more  nicely  prescribed  than  in  the  following  words : 

* I urge  you  not  to  be  too  unkind,  but  to  consider  carefully  your 
patient’s  super-abundance  or  means.  Sometimes  give  your  services 
for  nothing,  calling  to  mind  a previous  benefaction  or  present  satis- 
faction. And  if  there  be  an  opportunity  of  serving  one  who  is  a 
stranger  in  financial  straits,  give  full  assistance  to  all  such.  For 
where  there  is  love  of  man,  there  is  also  love  of  the  art.’ 

Here  then  we  have,  in  these  few  quotations,  sane  and 
ldncUy  recommendations  for  the  physician’s  life,  requiring 
of  him  a high  morality,  devotion  to  professional  secrecy, 
avoidance  of  jealousy,  willingness  to  confer  with  colleagues. 


THE  HIPPOCRATIC  IDEAL  477 

avoidance  of  undue  ‘show’,  and  kindness  to  patients  in  the 
matter  of  fees.  We  need  no  other  code. 

Disciples  of  the  Hippocratic  Method 
It  might  seem  invidious  to  select  from  the  pages  of  medical 
history  men  who  have  exemplified  the  Hippocratic  type 
above  their  fellows.  In  every  era,  although  there  were  dark 
gaps  in  the  Middle  Ages,  and  in  every  civilized  country 
there  have  been  physicians,  eminent  or  obscure,  who  have 
faithfully  pursued  the  old  ideal.  Sydenham  well  earned  Ins 
title  of  ‘the  English  Hippocrates’  in  his  professional  life 
and  by  his  endeavour  to  give  a true  description  of  the 
natural  history  of  diseases.  William  Heberden,  who  gave 
the  first  account  of  angina  pectoris  in  all  its  clinical  details, 
and  insisted  on  careful  note-taking,  was  of  similar  breed. 
Trousseau  and  Osier,  great  teachers  and  practitioners,  were 
of  the  same  genus.  But  countless  others  among  physicians 
and  surgeons  and  among  general  practitioners  of  the  lovable, 
cultured  type  of  Dr.  John  Brown — the  author  of  Hah,  and 
his  Friends — have  fulfilled  the  Hippocratic  behest.  Among 
our  own  colleagues  and  teachers  and  family  doctors  we 
could  name  not  a few  besides.  If  wc  look  beyond  the 
anecdotes  which  grew  around  John  Abemcthy  and  have 
given  him  a reputation  for  uncouthness,  wc  must  agree  to 
include  him  in  the  same  school.  Another  great  surgeon, 
Symc  of  Edinburgh,  accounted  Abemethy  the  finest  surgical 
mind  after  John  Hunter  and  Percival  Pott,  but  he  was  a 
physician  too,  a physiologist,  and  even  a psychologist,  for 
he  wrote  a well-reasoned  little  essay  on  the  Mind.  He  saw 
things  whole,  and  based  his  views  and  treatment  on  sound 
obseiwation  and  common  sense.  His  generosity  to  poor 
patients  is  proverbial  and  can  seldom  have  been  surpassed. 

The  Fotuue  of  Medicine 

How  shall  we  weld  the  methods  of  Hippocrates  and 
Harvey  to  obtain  the  fullest  benefits  of  both?  How  arc  wc 
to  combine  the  old  with  the  new  ? Experimental  medicine, 
full  of  gifts,  firing  the  imagination  and  claiming  the  industry 
of  the  younger  generations,  but  moving  ahead  with  too 


478  THE  HIPPOCRATIC  IDEAL 

little  co-ordination  and  control;  the  old  steady  observa- 
tional medicine,  no  less  scientific  in  careful  hands,  but  often 
betrayed  by  lack  of  accuracy  and  care ; and  the  art  of  prac- 
tice based  upon  an  admixture  of  these  sciences  with  human 
kindliness  and  vision  and  courage  and  much  restraint — 
how,  in  our  individual  and  professional  lifetime,  are  we  to 
accomplish  a wiser  use  and  application  of  these  three? 
IIow  again  are  we  to  modify  our  curriculum  and  examina- 
tion system  in  such  a way  as  to  lighten  the  burden  of  the 
student  and  yet  give  him  firmer  foundations  and  a broader 
view? 

For  myself  I should  like  to  appeal  for  better  opportunities 
for  observational  training  and  the  use  of  the  senses  in  field 
natural  history  during  the  school  period,  and  better  oppor- 
tunities for  continuing  the  education  of  the  senses  by 
parallel  clinical  study  of  the  healthy  and  the  sick  during 
the  pre-clinical  phases  of  medical  education.  Eyes,  hands, 
ears,  and  nose,  and  the  technique  of  history-taking,  require 
constant  utilization  and  free  scope.  To  quote  Dr.  John 
Brown: ' In  a word,  let  me  say  to  my  young  medical  friends, 
give  more  attention  to  steady  common  observation — the 
old  Hippocratic  aKpifieia,  exactness,  literal  accuracy,  pre- 
cision, niceness  of  sense ; what  Sydenham  calls  the  natural 
history  of  disease.  Symptoms  are  universally  available: 
they  are  the  voice  of  nature. . . . ’ 

Human  psychology,  in  its  daily  practical  bearings  (and 
more  than  half  of  practical  medicine  is  psychology),  must 
take  its  place  beside  a more  applied  and  less  elaborate  human 
anatomy,  physiology,  and  pathology.  Specialism  in  educa- 
tion (and  most  pre-clinical  and  extra-clinical  teachers  have, 
of  necessity,  the  specialist  outlook)  carries  with  it  the  same 
disadvantages  as  too  early  specialism  in  practice.  It  dis- 
courages the  free  use  of  the  senses  and  reasoned  correlation 
of  facts,  and  delays  the  growth  of  judgement,  which  is  the 
clinician’s  crowning  need.  If  we  are  to  breed  more  and 
better  specialists  it  is  also,  to  my  thinking,  essential  that 
we  should  preserve  a just  balance  by  breeding  more  and 
better  workers  in  the  field  of  general  medicine. 

In  the  domain  of  practice,  whether  we  come  eventually 


THE  HIPPOCRATIC  IDEAL  470 

to  a State  service  or  move  forward  in  our  present  paths,  we 
must  seek  to  temper  our  new  science  and  indispensable 
discoveries  with  what  our  fathers  possessed  in  better 
measure  than  we  do — the  old  Hippocratic  principles  of  art 
and  conduct.  In  every  branch  we  need  something  of  the 
philosophy  of  the  man  who,  with  all  his  vast  learning  and 
achievement,  was  humble  enough  to  realize,  as  his  most 
famous  aphorism  reminds  us,  that  ‘Life  is  short,  the  Art 
long,  opportunity  fleeting,  experience  treacherous,  and 
judgement  difficult*.  With  the  aid  of  such  wise  humility 
and  his  strong  exhortations  to  patient  research  and  a love 
both  of  truth  and  man,  we  shall  one  day  combine  the  new 
with  the  old,  resolving  present  difficulties,  and  raise  the 
standards  of  the  Science  and  Art  of  Medicine  to  a level  at 
present  beyond  our  vision. 

BIBLIOGRAPHY 

Adams,  Francis.  The  Genuine  It'orto  of  Hippocrates.  The  Sydenham 
Society,  London,  1840. 

Jones,  \V.  A.  S.,  and  Whittington,  E.  T.  Hippocrates.  The  Locb 
Classical  Library. 


INDEX  OF  AUTHORS 


Abercrombie,  J„  105,  117. 
Abemcthy,  J.,  477. 

Abraliams,  A.,  -08,  277. 
Abrahamson,  L.,  318,  319,  351,  35c. 
Adams,  F.,  470. 

Adams,  J.,  330. 

Addison,  W.,  1,  7,  0,  322,  433,  435, 
402. 

Allbutt,  Sir  T.  Clifford,  80,  84,  21 1, 
305,  31 C,  310. 

Aretaeos,  I6t,  160. 

Armstrong,  R.  R.,  272,  277. 

Each,  F..  419,  450. 

Ilacon,  F.,  1,  20. 

Banting,  Sir  F.,  18,  4C2. 

Rarber,  II.  IV.,  134,  150. 

Barclay,  A.  E.,  70,  34. 

Barclay,  P.  E.,  450.  400. 
Barrington,  F.  J.  II.,  251,  204. 
Bazctt,  II.  L..  82,  84. 

Beaumont,  IV.,  110,  123,  129. 
Bennett,  T.  I.,  78,  84,  07,  117,  133, 
150,  431,  435. 

Bolton,  C,,  431. 

Bradley,  IV.  II.,  454,  455,  4C0. 
Briggs,  J.  B-,  319,  330. 

Bright,  R.,  1,  7,  0, 11. 144. 150, 15j, 
100,  208,  439,  402. 

Brinton,  IV.,  120,  129. 

Broadbent,  Sir  IV.,  321. 

Brown,  J.,  477,  478. 

Bruce-Perry,  C.,  452,  450. 
Bucldand,  F.,  6,  10. 

Buerger,  L.,  355,  350. 

Cabot,  II.,  202,  204. 

Campbell,  J.  »I.  II.,  97,  117,  34l, 
340,  331,  350,  372. 

Cannon,  W.  B.,  120,  129. 

Carlson,  A.  J.,  54,  03,  80,  120, 129. 
Cecil,  R.  I..,  208,  27J,  272,  277. 
Chamberlain,  IV.  E.,  07,  117. 
Cherehewsky,  102,  107,  169,  181. 
Ciocco,  A.,  451,  459. 

Oatke,  A.  L-,  202,  204. 

Coburn..  A.  E...  453.  460. 

Conybeare,  J.  J.,  07,  117. 

Cooke,  A.  M.,  361. 

Coombs,  C.  T.,  348,  354,  356. 

Cope,  Z.,  39. 

Corrigan,  D.  J.,  300. 

Curling,  T.  B.,  195,  200. 

Daniel,  G.  H.,  452,  460. 

Darwin,  C.,  4,  5,  10,  18,  420,  429. 


Dean,  II.  R.,  421. 

Donovan.  G.  E.,  452, 400. 

Draper,  G.,  159,  427,  433,  435, 
4-11. 

Dudley,  S.  F.,  453,  400. 

Evans,  G.,  109,  300. 

Faber,  K.,  07,  117. 

Fabre,  II.,  0. 
fngge,  II.,  375. 

Fairley,  N.  IL,  114, 117. 

Fawcett,  J.,  413. 

Teasby,  IV.  R„  451.  460. 

Felton,  L.  D.,  265,  271. 

Fleincr,  W.,  102,  167,  169,  184. 
Fraenkel,  A.,  205. 

Fripp,  A.,  282. 

Cairdner,  IV.  T.,  3,  71. 

Garrod,  Sir  A.  E.,  159, 100, 427, 428, 
435. 

Gee,  S.,  157,  ICO. 

Glover,  J.  A.,  454, 460. 

Coiffon.  R.,  139, 150. 

Goodali,  J.  S-,  119, 129. 

Coodhart,  Sir  J.,  128, 129. 

Cowers,  Sir  IV.,  80, 82, 212, 392, 395, 
397. 

Green,  C.  A.,  453,  454,  460. 

Gull,  Sir  IV..  7,  15,  25,  28. 127, 129. 
138,  145,  150,  151,  160,  215,  229, 
287,  315,  318,  371,  375 

Haldane,  J.  S.,  460. 

Hare,  R„  454,  4 CO. 

Harvey,  1V„  1,  7,  18,  462,  477. 
Hawkins,  II.  P..  302,  107,  109,  171, 
183,  184. 

Head,  Sir  IL,  35,  53,  CO,  04.  65,  68, 
437. 

Heberden.  IV.,  1, 7,  8,  22,  40,  06,  68, 
105,  200,  295,  299,  303,  321,  325, 
335,  477. 

Ilelmholx,  IL  F.,  262,  234. 

Herrick,  IV.  IV.,  319,  35(1 
Hill,  N.  G.,  440.  459. 

Hilton,  J.,  38, 53, 55, 62, 05,  68, 189, 
192. 

Hippocrates,  2,  7,  11,  15,  23,  117, 
279,  439.  462. 

Hodgkin,  T.,  322.  462. 

Holland  Clarke.  P.  J.,  452,  460. 
Home,  Sir  336. 

Houghton,  IV.,  361. 


INDEX  OF  AUTHORS 


Ilovrship,  J„  102, 103, 107, 109, 175, 
181. 

Hudson,  IV.,  7. 

Hunter,  J.,  1,  10,  18,  93,  117,  303, 
330,  335,  477. 

Hunt,  Sir  A-  F.,  39, 53, 54, 55,  <58, 80, 
03,  06,  03,  00.  109,  117,  128,  110, 
149,  150,  102,  107,  109,  171,  170, 
184,  195,  200,  237,  301,  423,  427, 
428,  431,  435. 

Hutchinson,  J.,  420,  428,  431,  433. 
Huxley.  T.  H„  5,  10,  18,  50.  429, 
435. 

Jackson,  E.,  182,  184. 

Jamieson,  T.  II.,  157, 160. 

Janney,  J,  II.,  202,  201. 

Jenner,  E..  1,  7, 10. 18. 410. 
Johnson,  11.  S.,  272.  277. 

Jones,  IV,  A,  S.,  479. 

Kidd,  F„  254,  259,  20-1. 

Kilncr,  X».  T.,  114, 117. 

King-Lewis,  F.  L.,  450,  400. 
Kinsclla,  V.  J.,  100, 107. 

Knott,  F.  A.,  203,  20*. 

Laennee,  H.  T.  II.,  1. 7,  239,  430. 
Lafdlavr,  Sir  P.  P.,  410. 
Langdon-Brown,  Sir  \V.,  427. 
Latham,  P.  M.,  835. 

Laycock,  T..  25. 

Layton,  T.  11.,  33. 

Lennander,  K.  C.,  39,  S3,  55,  68. 
Lewis,  Sir  T.,  18,  50,  70,  278,  430, 


Lister,  Sir  \V„  1.  410. 

Lloyd,  N.  L-,  301. 

SIc.Mpine,  D„  3G0. 

McGlone,  B.,  82,  8 1. 

Mackenzie,  II.,  875. 

Mackenzie,  Sit  J.,  S3, 40, 53, 08,  295, 
835,  437. 

Mahomed,  P.  A.,  815,  817,  319. 

M alloc  h,  A.,  2C8,  277. 
Sfaoson-Bahr.  P.,  157,  ICO. 

Marcus,  M.,  65, 08. 

Marsh.  K-  B.,  101. 
ilatthews  Duncan,  J.,  108,  200. 
Medical  Research  Council,  432, 459. 
Miller,  II.,  150,  157,  200,  452.  439. 
Minot.  C.  IL,  402. 

Slowly,  IL  O.,  07, 117. 

Moore.  L.  V.,  453. 4G0. 

Moorhead,  T.  C..  318.  3t9, 35*,  850. 
Morgan,  O.  G„  8*8,  35*,  350. 
Motley,  J„  39. 


481 

Morris,  J.  N.,  418,  432,  453,  459, 
4C0. 

Moynllian,  Lord,  06,  09,  101,  102, 
103,  105,  117,  437. 

Nielsen,  N.  A.,  95, 117. 

Ord,  W.,  375. 

Oser,  L.,  151,  ICO, 

Osier,  Sir  IV.,  7,  835,  402,  477. 
Owen,  A.  \V.,  3 *9,  350. 

Fagct,  Sir  J.,  202, 210, 21 1, 818, 350. 
Panton,  F.  N.,  254,  20*. 

Parkinson,  J.  4-13,  450,  400. 

Pasteur,  L.,  402. 

Faterson,  II.,  150, 100. 

Pavlov,  1. 1\,  18. 120. 

Payne,  IV.  \\\,  70,  00,  214. 

Perkins,  II.,  ICO. 

Pickies,  IV.  N\,  431,  400. 

Pott,  I*.,  477. 

Poulton,  E.  I*.,  70,  00,  214,  210. 
Poynton,  F.  J.,  ISO,  100,  452,  400. 
Preston,  T.  \\\,  +10,  450. 

RachmilewiU,  M.,  301. 

Read,  F.  E.  SI.,  451,  459. 

Rhea,  L.  J.,  208. 277. 

Roberts,  J.  A.  Fraser,  432,  459. 
Robson,  W.  M.,  ioo,  200. 

Rollcston,  Sir  II.  D.,  427, 433. 

Ross.  J„  39,  53.  68. 

Roux,  J.  Ch.,  130, 143, 147. 

Rvffei.  J.  II.,  143. 
nyle,  J.  A.,  84,  117,  150,  277,  397, 
431,  435. 

Schmidt,  IL,  30. 

Schmidt,  van  N..  13*.  150. 

ScotL  H.  II.,  157,  ICO. 

ShoM,  A.  T.,  SOS,  SOt. 

Simpson,  J.  Y.,  105,  200. 

Sleslnger,  E,  C..  374. 

Smith,  It.  IX,  239. 

Smuts,  J.,  15,  20. 

Stacey  Wilson,  T.,  162,  16*.  107, 
169, 173.  163. 18*. 

Stewart,  51.  J.,  06,  117. 

Still,  C.  1\,  150,  ICO. 

Stocker,  J.,  20,  378. 

Sutton,  IL  <L,  15.  229,  317,  318. 
Sydenham,  T.,  7, 8, 11, 14, 439, 463, 
473,  477. 

Symonds,  Sir  Cliarles,  82. 231,  370. 
Symonds,  Sir  Charters,  472. 

Tauofg,  II.  IL,  451,  459. 

Thomson  AValker,  Sir  J.,  359. 
Thornton,  C.  IL,  4*9,  459. 


432  INDEX  OF  AUTHORS 


Tidy,  Sir  II.  L„  254, 201. 

Timbal,  L.,  147, 150. 

Titmuss,  It.  M„  418,  452,  453,  450, 
ICO. 

Trotter,  IV.,  70,  437. 

Trousseau,  A.,  1,  7,  477. 

Turner,  J\,  1C2, 107,  160, 184. 

Von  Nuys,  II.  G.,  07, 117. 

Venables,  J.  F.,  78,  84,  301. 

Warner,  E.  C.,  453,  4G0. 
Washbumc,  A.  L.,  120,  129. 
Woterfleld,  IL  L.,  207,  208,  277. 


Watcrton,  C.,  0. 

Waugli,  G.,  55,  08. 

Webb,  R.  A.,  421. 

Whipple,  G.  II.,  150,  ICO. 

Write,  C.,  0. 

Whittington,  E.  T.,  470. 

Wilkie,  Sir  D.  P.  D.,  04, 117. 
Wilks,  Sir  S.,  7,  27,  201,  315.  317. 

31 D,  300,  307,  402. 

Winterton,  F.  G.,  453,  4CO. 

Wright,  II.  D.,  234,  20 1. 

Yarrell,  W.,  0. 

Young,  M.,  452,  459. 


SUBJECT  INDEX 


Abscess,  ischto- rectal.  192. 
Aerophagy,  89. 

Allergy,  412. 

Anaemia,  pernicious,  433. 
Anaphylaxis,  412. 

Angina  abdominahs,  331. 

Cruris,  031. 

Angina,  anaemic,  S30. 

Pectoris,  321. 

Angor  nnimi,  79,  323. 

Anorexia,  118. 

Aphorisms,  Hippocratic,  403. 
Arrhythmia,  sinus,  299. 

Auricular  fibrillation,  293,  299. 
Auricular  flutter,  297. 

Bacillus  coll  communis. 

Infections  with,  231. 

Infections,  biliary,  235. 

Infections,  urinary,  231. 
Bacterhemia,  21 8,  231,  200. 
Bradycardia,  203- 
Bright’s  disease,  313. 

Cancer  phobia,  405. 

Coellac  disease,  150. 

Colitis,  rouco-memhiunous,  170, 176. 
Colon,  spastic,  102,  108. 
Appendicectomy  in,  172. 
Spasmodic  affections  of,  103. 
Constipation,  spastic,  102. 
Constitution,  423. 

Decubitus,  27. 

Diarrhoea,  after  gastro-jejunos- 
tomy,  137. 

Chronic,  139. 

Chylous,  145. 

Classification  of,  131. 

Colonic.  138. 

Fatty,  145,  I3t. 

Gastric.  133. 

Intestinal,  137. 

I ns  estimation  of,  132. 

Nervous,  147. 1*8. 

Pancreatic,  141. 

KectaJ,  133. 

With  elioiecystitU,  147. 
Diathesis,  42fl. 

Disease,  definition  of,  1 4, 

Natural  history  of,  1 1. 
Physiognomy  of,  25. 

Dying,  sense  of,  74,  79. 

Experiment,  17,  4.33. 

I’xtrasystoie*,  *JW. 


Fever,  staph)  lococcal,  215. 

Streptococcal,  233. 

Fistula,  gastra-eohe,  314. 
Flatulence,  So,  83. 

Gaits,  27,  23, 

Guarding,  59. 

Hearing,  30. 

Heartburn,  8fl,  89. 

Hiccups,  80,  01. 

Hunger-pain,  86,  87. 

Hyperalgesia,  59. 

Hyperpicsia,  305. 

Prognosis  of,  291,  813. 

Symptoms  of,  309. 

Lacteals,  obstruction  of,  1 SI. 

Meningism,  376. 

5fen£ngitis,  076. 

Migraine,  385. 

Apliasic,  397. 

Hemiplegic,  337. 

Vestibular,  333. 

Myx  oedema,  305. 

Naturalist,  functions  of,  4. 

Nausea,  74.  77. 

Neuroses,  cardiac,  211. 

Colonic,  203. 

Gastric,  207. 

Oesophageal,  205. 

Paroxysmal,  335. 

Rectal,  209. 

Vesical,  210. 

Viscera),  201. 

Neuroses,  visceral,  initiation  of,  203. 

Perpetuation  of.  201. 

Nosophobia,  308. 

Observation,  17. 

Oedema,  pulmonary,  344. 

Palo,  analysis  of.  42,  43.  44,  45,  46, 
70. 

Anginal.  57.  324.  327. 
Appendicular,  02. 

Arm.  53. 

Colonic.  74,  75,101. 

I>uodenal,  57. 

Call- bladder,  57.  60. 

Gastric,  57,  59. 

Intestinal.  57,  04. 


484  SUBJECT  INDEX 


Pain  (coni.): 

Referred,  52. 

Renal,  57,  C4. 

Scapular,  58. 

Shoulder,  61 . 

Study  of,  37. 

Testicular,  58. 

Ureteric,  57,  6-1. 

Uterine,  05. 

Visceral,  52. 

Visceral,  laws  of,  41. 

Physician,  functions  of,  7. 

Meaning  of,  2. 

Training  of,  If). 

Pneumonia,  lobar,  203. 

Mortality  In,  207. 

Prognosis  in,  207. 

Serum  in,  271. 

Prognosis,  278. 

Hippocrates  oo,  467. 

Pulse,  radial,  235. 

Alternating,  209. 

Bigeminal,  302. 

Dicrotic.  302. 

In  Addison’s  disease,  301. 

In  Aortic  stenosis,  301. 

In  Ilyperpiesla,  301. 

Paradoxical,  So3. 

Water-hammer,  800. 
Pulselessness,  302. 

Pyrexia,  obscure,  103. 

Rectum,  ball-valve  accumulations 
in,  192,  105. 

Carcinoma  of,  100. 

Examination  of,  185,  186. 
Regurgitation,  acid,  80,  00. 
Research,  430. 

Rheumatic  rever,  Morbidity,  450. 
Mortality,  418. 

Notification,  457. 

Social  Pathology,  410,  458. 

Sense,  clinical,  17. 

Senses,  training  of,  24. 

Septicaemia,  218,  234,  260. 

Sight,  25. 

Smell,  32. 

Specialism,  10. 

Sprue,  157. 

Status  anginosus,  829. 

Stoma,  ‘Dumping’,  114. 


Symptoms,  functions  of,  72. 
Gastric,  80. 

Nature  of.  72. 

Study  of,  CO. 

Syndrome,  Gower’*,  **e  Vasovagal 
attacks. 

Syphilophobia,  404. 

Tachycardia,  paroxysmal,  297. 
Tetany,  81, 15-1. 

Thrombophlebitis  migrans,  348. 
Thrombosis,  coronary,  329,  335. 
Touch,  29. 

Ulcer,  anal,  190. 

Ulcer,  anastomotic,  112, 

Ulcer,  duodenal,  03. 

Alkalosis  in,  110. 

Complications  of,  108. 

Course  of,  101, 

Diathesis  in,  426. 

Erosion  of  pancreas  iij,  107,  111. 
Haemorrhage  in,  102. 

Indications  for  surgery  in,  115. 
Influence  of  age,  08. 

Climate,  100. 

Constitution,  00. 

Environment,  100. 

Tocal  sepsis,  100. 

Mental  states,  101. 

Occupation,  08. 

Season,  101. 

Sex,  03. 

Tobacco,  100. 

Mortality  of,  103. 

Objective  signs  in,  107. 

Tain  in,  104. 

Perforation  in,  102. 

Prophylaxis  of,  116. 

Pyloric  stenosis  in,  103. 

Symptoms  of,  103. 
l/raemia  in,  1 10,  357. 

Vomiting  in,  105. 

Water-brash  in,  100. 

Uraemia,  gastric,  110,  357,  362. 

Pro  static,  357. 

Vasovagal  attacks,  80,  81,  330,  392. 
Vertigo,  38S,  389. 

Vomiting,  riaous  cycle,  ll-l. 

Watet-brash,  86,  87,  00,  106.